{"id": "pmc-13132212-conclusion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-conclusion", "source": "PubMed Central open-access full text", "pmcid": "PMC13132212", "pmid": "42060588", "doi": "10.1371/journal.pone.0348079", "title": "Type 1 and Type 2 diabetes in the UK press: A diachronic corpus-based analysis", "journal": "PLOS One", "publication_year": 2026, "citation": "Sara Vilar-Lluch, Dawn Knight · (2026) · \"Type 1 and Type 2 diabetes in the UK press: A diachronic corpus-based analysis\" · PLOS One · doi: 10.1371/journal.pone.0348079 · PMCID: PMC13132212 · PMID: 42060588", "question": "What does the published research conclude about \"Type 1 and Type 2 diabetes in the UK press: A diachronic corpus-based analysis\"? Cite a peer-reviewed source.", "answer": "UK news media shows competing medical and free will discourses in T1D and T2D reports, and a gradual increase in the use of language recommended by diabetes guidelines, albeit the latter is not mirrored by a similar decrease in dispreferred language. Although the newspaper articles include references to diabetes types, references to diabetes ‘in general’ are common, supporting reported concerns of individuals living with T1D/T2D [ 13 , 17 ] and echoing findings of news media studies in other contexts (e.g., [ 20 ] in New Zealand). In the Diabetes UK News Media Corpus, general uses of ‘diabetes’ occur when reporting risks common for both diabetes types, but also stand metonymically for one type, ultimately relying on readers’ ability to discern the type of diabetes discussed (see example 10).\n\nAs observed in previous studies of diabetes representation in news media (e.g., [ 20 , 21 , 28 , 35 , 36 ]), medical discourse is also prominent in the corpus examined. In the Diabetes UK News Media Corpus, the medical discourse is used in articles that mention both diabetes types but is particularly common for T1D. The medical discourse alludes to medical causes and medicines as management strategies. It is also enacted by referring to T1D and T2D in the context of other medical conditions, either by portraying some observed similarity (specially for T1D), or by presenting diabetes as the causal factor (specially for T2D). Causal relations or common risk factors are sometimes explicitly stated. Other times, however, associations between medical conditions appear unclear, which can lead to erroneous inferences of causality or evaluations by association.\n\nThe medical discourse can contribute to reduce moral blame and stigma associated with T2D, popularly regarded as a consequence of unhealthy diet and sedentary lifestyle. While the medical discourse is adopted, discussions around the social determinants of health (SDH) [ 49 ] that may impact on diabetes development and management were not frequently featured in the articles. SDH are conditions in which people are born or live that, although not directly related to health, affect individuals’ health, such as income, food security, education or social inclusion [ 49 – 50 ]. Omission of societal factors is common in news media reporting of diabetes (e.g., [ 20 , 37 , 38 ]). Overlooking SDH ultimately contributes to depict diabetes (both types) as an individual problem, and diabetes management as an individual responsibility. The collocation analysis did not reveal any discussion around the affordability of healthy diets and the ongoing UK food crisis [ 51 – 53 ], neither did it include references to the affordability of adopting active lifestyles across demographics, or debates on economic policies to promote healthy eating. Instances referring to the economic and emotional burden of living with diabetes (T1D or T2D) have not been observed in the analysis.\n\nThe medical discourse competes with an underlying discourse of free will, particularly observed for T2D. References to lifestyle and diet do not predominate among the management strategies identified in the corpus, contrasting with previous studies which reported recurrent associations of T2D with individual behaviours and lifestyle changes as remedies (e.g., [ 20 , 35 , 36 ]). However, lifestyle (including dietary habits) features in descriptions of causes leading to T2D and in associations of T2D with obesity/overweight. The absence of discussions around factors leading to obesity/overweight (e.g., genetic, ill health, socioeconomic) can contribute to reinforce its association with over-indulgence; by inference, T2D is implicitly depicted as an individual moral failure. T1D is not associated with negative moral judgements, and autoimmune and genetic causes are emphasised, sometimes including explicit contrasting descriptions with T2D. Verbs conveying control are common in T1D reporting. These verbs depict T1D as requiring high individual responsibility, evoking positive assessments of those that manage it successfully. However, failure to refer to factors that hinder T1D management implicitly blames the individuals (or their parents/carers) for health complications.\n\nOverall, this analysis has shown that UK news media reporting on T1D and T2D reflects competing societal discourses on health and wellbeing. The medical discourse promotes current scientific understanding and avoids moral blaming. The avoidance of discussions around societal structures (societal frames) in reporting management strategies and (T2D) causes, however, places health-preventive actions in the individual responsibility exclusively, overseeing prevalent inequalities that may contribute to develop T2D, or that interfere with T1D and T2D management.\n\n— Source (conclusions, peer-reviewed): Sara Vilar-Lluch, Dawn Knight · (2026) · \"Type 1 and Type 2 diabetes in the UK press: A diachronic corpus-based analysis\" · PLOS One · doi: 10.1371/journal.pone.0348079 · PMCID: PMC13132212 · PMID: 42060588\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12811412-conclusion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-conclusion", "source": "PubMed Central open-access full text", "pmcid": "PMC12811412", "pmid": "41552835", "doi": "10.1155/pedi/5539725", "title": "From Pathophysiology to Treatment: Contemporary Approaches to CFRD in the Pediatric and Adolescent Population", "journal": "Pediatric Diabetes", "publication_year": 2026, "citation": "Dogus Vuralli · (2026) · \"From Pathophysiology to Treatment: Contemporary Approaches to CFRD in the Pediatric and Adolescent Population\" · Pediatric Diabetes · doi: 10.1155/pedi/5539725 · PMCID: PMC12811412 · PMID: 41552835", "question": "What does the published research conclude about \"From Pathophysiology to Treatment: Contemporary Approaches to CFRD in the Pediatric and Adolescent Population\"? Cite a peer-reviewed source.", "answer": "CFRD represents a unique and increasingly important aspect of CF care as life expectancy continues to improve. While CFRD poses significant clinical challenges, it is also highly manageable with early detection, individualized insulin treatment, and continuous monitoring. The advent of CFTR modulators and the emergence of novel diabetes technologies have created new opportunities to optimize glycemic control and enhance quality of life for PwCFRD. Ongoing research evaluating the long‐term effects of CFTR modulators on insulin secretion and glycemic control, investigating noninsulin therapies, developing predictive biomarkers, and refining diagnostic tools will be instrumental in shaping future management strategies. Ultimately, integrating these advances into routine clinical care will be key to preserving pulmonary function, nutritional status, and quality of life, ensuring that PwCF can continue to thrive throughout their lifespan.\n\n— Source (conclusions, peer-reviewed): Dogus Vuralli · (2026) · \"From Pathophysiology to Treatment: Contemporary Approaches to CFRD in the Pediatric and Adolescent Population\" · Pediatric Diabetes · doi: 10.1155/pedi/5539725 · PMCID: PMC12811412 · PMID: 41552835\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-11045978-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC11045978", "pmid": "38681763", "doi": "10.3389/fendo.2024.1353543", "title": "Challenges in the postsurgical recovery of cushing syndrome: glucocorticoid withdrawal syndrome", "journal": "Frontiers in Endocrinology", "publication_year": 2024, "citation": "Catherine D. Zhang, Adriana G. Ioachimescu · (2024) · \"Challenges in the postsurgical recovery of cushing syndrome: glucocorticoid withdrawal syndrome\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2024.1353543 · PMCID: PMC11045978 · PMID: 38681763", "question": "Summarize the abstract of the paper titled \"Challenges in the postsurgical recovery of cushing syndrome: glucocorticoid withdrawal syndrome\".", "answer": "Glucocorticoid withdrawal syndrome is a challenging clinical phenomenon that can complicate the postsurgical recovery of Cushing syndrome. It is characterized by physical tolerance and dependence to supraphysiologic glucocorticoid exposure during active Cushing syndrome followed by the abrupt decline in cortisol levels after surgical treatment. The symptoms of glucocorticoid withdrawal often overlap with those of postoperative adrenal insufficiency and can be difficult for patients to cope with and for clinicians to treat. This mini review will discuss the clinical characteristics, pathophysiology, and management of glucocorticoid withdrawal syndrome while highlighting recent data in the field.\n\n— Source (abstract, peer-reviewed): Catherine D. Zhang, Adriana G. Ioachimescu · (2024) · \"Challenges in the postsurgical recovery of cushing syndrome: glucocorticoid withdrawal syndrome\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2024.1353543 · PMCID: PMC11045978 · PMID: 38681763\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12582498-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC12582498", "pmid": "41183121", "doi": "10.1371/journal.pone.0334163", "title": "Identification of Seven in absentia homolog 2 as a potential efferocytosis-related biomarker in diabetic foot ulcers", "journal": "PLOS One", "publication_year": 2025, "citation": "Jiangli Zhao, Xuchen Liu, Qingyuan Sun, et al. · (2025) · \"Identification of Seven in absentia homolog 2 as a potential efferocytosis-related biomarker in diabetic foot ulcers\" · PLOS One · doi: 10.1371/journal.pone.0334163 · PMCID: PMC12582498 · PMID: 41183121", "question": "Summarize the abstract of the paper titled \"Identification of Seven in absentia homolog 2 as a potential efferocytosis-related biomarker in diabetic foot ulcers\".", "answer": "Wound of diabetic foot ulcers (DFU) is chronic and hard to heal, characterized by impaired inflammatory response, dysfunction of keratinocyte and endothelial cells and improper removal of dying cells. Efferocytosis, as a trigger for phenotype switch of macrophages, plays a critical role in diabetic foot wound healing. Here, we showed the effect of efferocytosis in wound healing of diabetics and identified seven in absentia homolog 2 (SIAH2) as a potential efferocytosis-related biomarker.\n\nBlood and skin samples were collected from 20 patients diagnosed type II diabetes at Qilu Hospital of Shandong University. Efferocytosis related genes in DFU were identified based on GSE147890 , GSE80178 datasets as well as RNA-seq data of blood samples. Enrichment analysis, clustering analysis and protein-protein interaction network analysis were conducted based on the efferocytosis related genes in DFU. An array diagram was constructed and survival analysis of DFU was performed based on the associated clinical data. Single-cell sequencing data analysis combined with experiments in vitro, we analyzed the role of SIAH2 in wound healing of DFU as well as its correlation with efferocytosis signal.\n\nOverall efferocytosis and SIAH2 expression level were increased in DFU blood and tissue samples and associated with poor survival in patients. Single-cell analysis revealed elevated SIAH2 expression is positively associated with keratinocyte migration, angiogenesis and efferocytosis of macrophage in wound healing of DFU. SIAH2 involved in efferocytosis-related cell-to-cell communication, especially in “internalization” and “digestion” signals.\n\nSIAH2 was identified to be one of the key efferocytosis genes and associated with poor prognosis of DFU. Protective upregulation of SIAH2 was involved in angiogenesis, keratinocyte migration and cell-to-cell communication mediated by efferocytosis in DFU wound healing.\n\n— Source (abstract, peer-reviewed): Jiangli Zhao, Xuchen Liu, Qingyuan Sun, et al. · (2025) · \"Identification of Seven in absentia homolog 2 as a potential efferocytosis-related biomarker in diabetic foot ulcers\" · PLOS One · doi: 10.1371/journal.pone.0334163 · PMCID: PMC12582498 · PMID: 41183121\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13051869-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC13051869", "pmid": "41933922", "doi": "10.1155/bmri/5408596", "title": "Correlation Analysis of Lower Limb Contrast‐Enhanced Ultrasound Findings With Serum VEGF and CXCL‐12 Levels in a Rabbit Model of Diabetic Foot", "journal": "BioMed Research International", "publication_year": 2026, "citation": "Yuzhong Wang, Tianlin Gao, Hong Zhou, et al. · (2026) · \"Correlation Analysis of Lower Limb Contrast‐Enhanced Ultrasound Findings With Serum VEGF and CXCL‐12 Levels in a Rabbit Model of Diabetic Foot\" · BioMed Research International · doi: 10.1155/bmri/5408596 · PMCID: PMC13051869 · PMID: 41933922", "question": "What did the discussion section of the paper \"Correlation Analysis of Lower Limb Contrast‐Enhanced Ultrasound Findings With Serum VEGF and CXCL‐12 Levels in a Rabbit Model of Diabetic Foot\" cover?", "answer": "Since skeletal muscle plays an important role in glucose metabolism, the occurrence of microcirculatory disorders will seriously affect the control of glucose metabolism in diabetic patients, thereby aggravating glucose metabolism disorders [ 22 ]. Currently, there are few dynamic and noninvasive methods for evaluating skeletal muscle microcirculation. Dynamic contrast‐enhanced magnetic resonance imaging and special sequences of magnetic resonance imaging can meet the requirements of dynamic evaluation and have good repeatability. They can be used to measure the maximum PI of the contrast agent and the TTP, enabling quantitative analysis of muscle microcirculation for the assessment of skeletal muscle perfusion [ 23 , 24 ]. However, this method has not been widely used in clinical practice yet. CEUS is a relatively noninvasive examination method that can real‐time evaluate the microcirculatory perfusion and blood flow distribution of the limbs. The blood flow velocity in blood vessels can be quantitatively expressed through the process of contrast agent perfusion and clearance, and it has been widely used in the detection and quantification of perfusion changes in muscle tissue and visceral tissue [ 25 , 26 ]. In this study, CEUS quantitative software was used to record the TIC during the contrast process. Among them, the blood flow volume during the microcirculatory filling phase can be reflected by PI and AUC; whereas TTP reflects the time efficiency of the contrast agent perfusing in the tissue and reaching the maximum enhancement, thereby reflecting the filling speed of the tissue microcirculation. The results showed that TTP, PI, and AUC increased sequentially in the normal stage, DM stage, and DFU stage, with statistically significant differences. However, TTP showed the most significant difference during the establishment of the diabetic foot model, and PI and AUC showed the most significant changes during the establishment of the DM model. The distinct patterns of parameter change across stages likely reflect a shifting pathophysiological dominance during the progression of diabetic microangiopathy in our acute model. Critically, this acute model may predominantly capture the early, dynamic phase of diabetic microvascular dysfunction, which is characterized by hemodynamic dysregulation and compensatory responses, rather than the end‐stage structural rarefaction seen in chronic disease. In the DM stage, the significant increases in PI and AUC may primarily indicate early functional disturbances in the local skeletal muscle microvasculature [ 27 ]. These include increased microvascular permeability and impaired venular outflow, leading to local pooling and delayed clearance of the contrast agent. This represents a state of hemodynamic dysregulation and functional decompensation within the muscle bed itself, effectively a pathological “hyper‐perfusion” state due to leakage and stasis, not adequate nutrient delivery [ 28 ].\n\nThe transition to the DFU stage is marked by the most dramatic prolongation of TTP. This suggests the superimposition of a new, dominant hemodynamic insult: significant inflow obstruction. Although progressive local capillary stenosis contributes [ 29 ], the extreme TTP prolongation strongly implies a major increase in upstream resistance [ 30 , 31 ], likely originating from the severely compromised distal microcirculation of the foot induced by the ulcer model, which aligns with the established concept of distal microvascular occlusion in diabetic foot pathology [ 32 ]. Thus, the DFU stage evolves into a state of severe perfusion failure characterized by the synergy of persistent local microvascular dysfunction and acute distal inflow obstruction.\n\nThis pathophysiological progression—from early dysregulation to late obstruction—provides a coherent framework to interpret the CEUS findings in our DM model. The observed “hyper‐perfusion” pattern (elevated PI/AUC) is interpreted as a specific form of early microcirculatory failure. In diabetic neuropathy, loss of sympathetic tone and pathological opening of arteriovenous shunts can lead to a state of “non‐nutritive hyperemia,” where total blood flow increases at the expense of nutritive capillary perfusion [ 33 ]. This classic hemodynamic derangement aligns with our hypothesis of early functional decompensation and directly explains the elevated PI and AUC due to increased but maldistributed flow.\n\nThe pattern of elevated PI and AUC observed in our DM animal model, along with the subsequent TTP prolongation in DFU, provides a dynamic depiction of microvascular evolution. Our acutely induced model, focusing on proximal skeletal muscle (gastrocnemius), captures the early neurogenic and hemodynamic phase of diabetic microangiopathy, characterized by dysregulated flow and shunting [ 33 , 34 ]. This phase may represent a critical transitional window in the natural history of the disease. Clinical studies often assess distal beds in patients with long‐standing diabetes, where structural changes and fixed hypoperfusion are predominant [ 35 ]. Therefore, our model offers a complementary perspective, illuminating the earlier functional disturbances that precede the well‐documented late‐stage structural ablation. The dynamic evolution of CEUS parameters observed here underscores their potential utility as biomarkers for staging disease progression and identifying early intervention points, which warrants further translational investigation.\n\nThe serum dynamics of VEGF and CXCL‐12 observed in this study—significantly elevated in DM and slightly declined yet still elevated in early DFU—can be interpreted within a dynamic “compensation‐to‐decompensation” framework of diabetic microangiopathy.\n\n— Source (discussion, peer-reviewed): Yuzhong Wang, Tianlin Gao, Hong Zhou, et al. · (2026) · \"Correlation Analysis of Lower Limb Contrast‐Enhanced Ultrasound Findings With Serum VEGF and CXCL‐12 Levels in a Rabbit Model of Diabetic Foot\" · BioMed Research International · doi: 10.1155/bmri/5408596 · PMCID: PMC13051869 · PMID: 41933922\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-9577902-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC9577902", "pmid": "36253014", "doi": "10.1136/bmjdrc-2022-003010", "title": "Metabolomic markers of glucose regulation after a lifestyle intervention in prediabetes", "journal": "BMJ Open Diabetes Research & Care", "publication_year": 2022, "citation": "Magdalena del Rocio Sevilla-Gonzalez, Alisa K Manning, Kenneth E Westerman, et al. · (2022) · \"Metabolomic markers of glucose regulation after a lifestyle intervention in prediabetes\" · BMJ Open Diabetes Research & Care · doi: 10.1136/bmjdrc-2022-003010 · PMCID: PMC9577902 · PMID: 36253014", "question": "Summarize the abstract of the paper titled \"Metabolomic markers of glucose regulation after a lifestyle intervention in prediabetes\".", "answer": "Disentangling the specific factors that regulate glycemia from prediabetes to normoglycemia could improve type 2 diabetes prevention strategies. Metabolomics provides substantial insights into the biological understanding of environmental factors such as diet. This study aimed to identify metabolomic markers of regression to normoglycemia in the context of a lifestyle intervention (LSI) in individuals with prediabetes.\n\nWe conducted a single-arm intervention study with 24 weeks of follow-up. Eligible study participants had at least one prediabetes criteria according to the American Diabetes Association guidelines, and body mass index between 25 and 45 kg/m 2 . LSI refers to a hypocaloric diet and >150 min of physical activity per week. Regression to normoglycemia (RNGR) was defined as achieving hemoglobin A1c (HbA1c) <5.5% in the final visit. Baseline and postintervention plasma metabolomic profiles were measured using liquid chromatography-tandem mass spectrometry. To select metabolites associated with RNGR, we conducted the least absolute shrinkage and selection operator-penalized regressions.\n\nThe final sample was composed of 82 study participants. Changes in three metabolites were significantly associated with regression to normoglycemia; N-acetyl-D-galactosamine (OR=0.54; 95% CI 0.32 to 0.82), putrescine (OR=0.90, 95% CI 0.81 to 0.98), and 7-methylguanine (OR=1.06; 95% CI 1.02 to 1.17), independent of HbA1c and weight loss. In addition, metabolomic perturbations due to LSI displayed enrichment of taurine and hypotaurine metabolism pathway (p=0.03) compatible with biomarkers of protein consumption, lower red meat and animal fats and higher seafood and vegetables.\n\nEvidence from this study suggests that specific metabolomic markers have an influence on glucose regulation in individuals with prediabetes after 24 weeks of LSI independently of other treatment effects such as weight loss.\n\n— Source (abstract, peer-reviewed): Magdalena del Rocio Sevilla-Gonzalez, Alisa K Manning, Kenneth E Westerman, et al. · (2022) · \"Metabolomic markers of glucose regulation after a lifestyle intervention in prediabetes\" · BMJ Open Diabetes Research & Care · doi: 10.1136/bmjdrc-2022-003010 · PMCID: PMC9577902 · PMID: 36253014\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12583124-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12583124", "pmid": "40847068", "doi": "10.1038/s41366-025-01889-0", "title": "Sensor-based evaluation of intermittent fasting regimes: a machine learning and statistical approach", "journal": "International Journal of Obesity (2005)", "publication_year": 2025, "citation": "Nico Steckhan, Tanja Manlik, Tillmann Int-Veen, et al. · (2025) · \"Sensor-based evaluation of intermittent fasting regimes: a machine learning and statistical approach\" · International Journal of Obesity (2005) · doi: 10.1038/s41366-025-01889-0 · PMCID: PMC12583124 · PMID: 40847068", "question": "What is the published background on \"Sensor-based evaluation of intermittent fasting regimes: a machine learning and statistical approach\"? Cite a peer-reviewed source.", "answer": "In clinical research, the data interpretation relies heavily on study compliance, meaning the extent to which participants adhere to the study protocol [ 1 ]. This is crucial in human studies where self-reporting over extended periods is required.\n\nCommon methods for measuring compliance include clinician impressions, patient interviews, prescription records, monitoring devices, and pharmacological markers. Patient interviews are straightforward and cost-effective, while pharmacological markers provide objective assessments but require ethical consideration [ 2 ].\n\nFasting studies often monitor ketone levels from urine, blood, or use newly developed breath ketone monitors to objectively measure adherence, but these methods require active participation and ketone increase is under the detection limit upon short fasting duration such as 16:8 fasting. Conversely, video surveillance or clinic-based meal consumption methods lack blinding [ 3 ]. Alternatively, participants may use photo and text food diaries [ 4 , 5 ] or log fasting times to track adherence.\n\nMobile and wearable technologies, including accelerometers, glucose monitors, and heart rate monitors, are increasingly used to monitor health-related parameters. Type 2 diabetes, the most common and preventable form of diabetes, is frequently studied [ 6 ]. Despite challenges in wearable technologies for dietary intake, such as transient signal loss and inaccurate calorie estimations [ 7 ], recent advancements in mobile sensors have improved the timeliness of dietary information. Continuous glucose monitoring (CGM) and activity tracking enable passive, unobtrusive data collection, enhancing compliance, reducing participant burden, and generating vast amounts of dynamic data, which are well-suited for advanced machine learning applications. Integrating data and machine learning in clinical research can predict diabetes risk and detect early signals of glucose metabolism disorders [ 8 – 10 ].\n\nTherefore, the primary aim of this study was to develop and assess the performance and applicability of different models utilizing sensor data to determine dietary adherence, e.g. the adherence of eating duration and the timely adherence regarding specific time-frames for eating within the context of intermittent fasting.\n\n— Source (introduction, peer-reviewed): Nico Steckhan, Tanja Manlik, Tillmann Int-Veen, et al. · (2025) · \"Sensor-based evaluation of intermittent fasting regimes: a machine learning and statistical approach\" · International Journal of Obesity (2005) · doi: 10.1038/s41366-025-01889-0 · PMCID: PMC12583124 · PMID: 40847068\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12949369-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC12949369", "pmid": "41761628", "doi": "10.1002/dmrr.70146", "title": "Association of Physical Activity and Socioeconomic Status With Glycaemic Control in Adults With Type 1 Diabetes: A Cross‐Sectional Study Using CGM Data", "journal": "Diabetes/Metabolism Research and Reviews", "publication_year": 2026, "citation": "Fernando Sebastian‐Valles, Rafael Simó, Jose Alfonso Arranz Martín, et al. · (2026) · \"Association of Physical Activity and Socioeconomic Status With Glycaemic Control in Adults With Type 1 Diabetes: A Cross‐Sectional Study Using CGM Data\" · Diabetes/Metabolism Research and Reviews · doi: 10.1002/dmrr.70146 · PMCID: PMC12949369 · PMID: 41761628", "question": "What did the discussion section of the paper \"Association of Physical Activity and Socioeconomic Status With Glycaemic Control in Adults With Type 1 Diabetes: A Cross‐Sectional Study Using CGM Data\" cover?", "answer": "The main finding of this study is that physical activity is associated with clinically meaningful improvements in CGM‐derived glycaemic control and cardiometabolic profile in adults with type 1 diabetes, and these benefits appear consistent across socioeconomic strata. Specifically, both physical activity and SES were independently associated with TIR, TITR, and HbA1c, and we found no evidence of an SES‐by‐physical activity interaction, indicating that the glycaemic benefits of physical activity were comparable across socioeconomic strata. Importantly, our mediation framework indicates that differences in physical activity levels may contribute to the SES gradient in TIR, thus suggesting that physical activity could be a feasible and cost‐effective target to attenuate SES‐related glycaemic disparities within a universal public healthcare context. Taken together, these findings support a clear equity‐oriented message: even in a setting with publicly funded CGM, socioeconomic differences in glycaemic outcomes persist and, therefore, behavioural intervention through physical activity promotion seems warranted.\n\nThese results align with prior studies documenting the metabolic benefits of exercise in people with T1D, including improved glycaemic outcomes and reduced cardiovascular risk [ 1 , 28 , 29 ]. However, our study builds upon existing evidence by using objective CGM‐based glucose metrics and applying a formal mediation framework, enabling quantification of the specific contribution of physical activity to SES‐related disparities. Unlike prior studies conducted in predominantly privately insured populations [ 14 , 15 ], our data were collected within a universal public healthcare setting, which enhances its generalisability to systems where structural inequities might be mitigated through policy. Moreover, by incorporating TITR alongside TIR and HbA1c, we provide a granular description of glycaemic improvements that is directly interpretable for clinical practice and current CGM targets.\n\nFrom a clinical perspective, the observed effects of physical activity on TIR (+8% points) and HbA1c (−0.47%, [–5 mmol/mol]) were both statistically and clinically significant, even after adjusting for SES and multiple covariates. Moreover, participants in the highest activity quartile had a 16% lower daily insulin requirement and more favourable lipid parameters, including lower triglycerides and remnant cholesterol. These secondary findings are directionally consistent with the expected physiological effects of exercise (improved insulin sensitivity and cardiometabolic risk profile) and reinforce the plausibility and coherence of the primary CGM‐based associations. This is particularly relevant given the growing evidence from Mendelian randomisation studies supporting a causal relationship between remnant cholesterol and cardiovascular disease [ 30 , 31 ], and its association with microvascular complications such as diabetic nephropathy, retinopathy [ 32 ], and foot disease in T1D [ 33 ]. At the physiological level, exercise enhances insulin sensitivity and mitigates oxidative stress and mitochondrial dysfunction, both of which are frequent findings in individuals with poorly controlled T1D [ 34 , 35 , 36 ]. Notably, studies in physically active older adults with well‐controlled T1D have reported preserved or even better mitochondrial function compared to non‐diabetic controls [ 37 ]. Exercise has also been associated with prolonged partial remission (‘honeymoon period’) after T1D onset, suggesting a protective effect on β‐cell function [ 38 ].\n\nA central contribution of this study is the integration of socioeconomic context with CGM outcomes to address a clinically actionable question: does physical activity confer similar glycaemic benefits across SES strata? The absence of a significant SES × physical activity interaction, together with the progressive increase in TIR across physical activity levels, suggests that the association between physical activity and glycaemic control is broadly consistent across socioeconomic strata. This is important because it supports the potential scalability of physical activity interventions without assuming differential effectiveness depending on SES. At the same time, the four‐way decomposition indicated a significant pure indirect effect, with approximately one‐quarter of the total association between SES and TIR explained by physical activity differences. This quantitative estimate provides a pragmatic framework for intervention design: reducing SES gaps in physical activity may translate into measurable improvements in glycaemic equity, even when technological access to CGM is universal.\n\nAs a minor caveat, our data showed a slight increase in TBR and number of hypoglycaemic episodes among individuals with the highest levels of physical activity; however, this was not accompanied by a longer duration of hypoglycaemic episodes. This finding could be explained by the widespread use of CGM alarms, which have been shown to mitigate exercise‐induced hypoglycaemia [ 39 ]. From a clinical standpoint, these results reinforce the need to pair physical activity counselling with structured education on insulin and carbohydrate adjustments around exercise, particularly for individuals with higher activity levels.\n\nDespite all these benefits, adherence to physical activity remains suboptimal, often limited by fear of hypoglycaemia, lack of professional support, inadequate access to safe environments, and low confidence in insulin adjustments around exercise [ 3 , 7 ]. Our findings imply that interventions aimed at promoting physical activity could improve glycaemic control across SES groups and serve as a powerful tool to reduce SES‐related health disparities. Moreover, the observed improvements in lipid profile—particularly reductions in triglycerides and remnant cholesterol, and increases in HDL—suggest a meaningful potential to lower cardiovascular risk. In parallel, the substantial reduction in insulin requirements among physically active individuals may translate into significant economic savings for both patients and healthcare systems, particularly in resource‐constrained settings. Given that many of the reported barriers are not unique to people with T1D [ 40 ] but are also common in the general population, scalable community‐based interventions‐such as supervised group programs, infrastructure enhancements, and digital support tools‐could be adapted and deployed effectively to promote physical activity in this vulnerable population. From an equity perspective, our findings support prioritising interventions that lower practical barriers to physical activity (tailored exercise education, accessible community programmes, and safe environments), which may complement technology‐access policies by addressing behavioural and environmental drivers of SES‐related differences in glycaemic outcomes.\n\nThis study has several limitations that should be acknowledged. Physical activity was assessed using a self‐reported questionnaire (IPAQ) rather than an accelerometer‐based measure, potentially overestimating activity levels [ 41 ]. As previously reported, IPAQ‐based estimates may overestimate true activity levels and are subject to recall and social desirability bias, which could have led to exposure misclassification and attenuation or inflation of associations. Notably, if measurement error in physical activity is largely non‐differential with respect to CGM outcomes, it would be expected to bias associations towards the null, suggesting that the observed estimates may be conservative. Second, we lacked information on certain potential confounders and contextual factors ‐such as alcohol intake and hypertension status‐ that may be associated with both physical activity and glycaemic outcomes. Third, the observed relationships between SES and physical activity may be affected by residual confounding from unmeasured individual‐ and neighbourhood‐level determinants (e.g., educational attainment, occupational characteristics, built environment, or health literacy), which could bias mediation estimates. In addition, SES was proxied using area‐level mean annual net income at the census‐tract level rather than individual‐level socioeconomic indicators. Although area‐based measures are widely used and correlate with deprivation indices, they may not fully capture within‐area heterogeneity and can introduce ecological misclassification. In principle, multilevel (hierarchical) modelling accounting for clustering by census tract could further disentangle individual‐ and area‐level effects; however, prior works [ 42 , 43 , 44 , 45 , 46 ] support the use of neighbourhood socioeconomic indicators as informative proxies for individual socioeconomic context in cardiometabolic research. We did not have complete, standardised CGM summaries over the preceding 12 months for all participants; therefore, we could not examine whether associations were consistent when using annual average CGM metrics, which would be valuable to reduce short‐term variability and better address temporality. Finally, the cross‐sectional design limits causal inference and temporality, particularly for mediation analyses, and reverse causation cannot be excluded (e.g., better glycaemic control enabling higher physical activity). Prospective longitudinal studies and intervention designs are therefore needed to confirm the directionality and magnitude of these associations. Accordingly, our mediation findings should be interpreted as quantifying associations under stated assumptions rather than as definitive causal effects.\n\nIn conclusion, physical activity is associated with better glycaemic and lipid control and lower insulin requirements in adults with T1D. Differences in physical activity account for nearly one‐fourth of the SES effect on glycaemic outcomes, and its benefits are consistent across income strata. Promoting physical activity and removing barriers to exercise might improve clinical outcomes, reduce healthcare costs, and help mitigate SES‐related disparities in T1D management. Future longitudinal and interventional studies should examine whether an increase in physical activity ‐particularly in lower‐SES contexts‐will result in sustained improvements in CGM targets and a reduction in SES‐related glycaemic outcomes.\n\n— Source (discussion, peer-reviewed): Fernando Sebastian‐Valles, Rafael Simó, Jose Alfonso Arranz Martín, et al. · (2026) · \"Association of Physical Activity and Socioeconomic Status With Glycaemic Control in Adults With Type 1 Diabetes: A Cross‐Sectional Study Using CGM Data\" · Diabetes/Metabolism Research and Reviews · doi: 10.1002/dmrr.70146 · PMCID: PMC12949369 · PMID: 41761628\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12747025-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12747025", "pmid": "41465900", "doi": "10.1097/MD.0000000000046758", "title": "Lipid metabolism in type 1 and type 2 diabetes: A comparative cross-sectional study", "journal": "Medicine", "publication_year": 2025, "citation": "Fatemah Saleh Bin Saleh, Ahmed R. Alibrahim, Awad S. Alshahrani, et al. · (2025) · \"Lipid metabolism in type 1 and type 2 diabetes: A comparative cross-sectional study\" · Medicine · doi: 10.1097/MD.0000000000046758 · PMCID: PMC12747025 · PMID: 41465900", "question": "What is the published background on \"Lipid metabolism in type 1 and type 2 diabetes: A comparative cross-sectional study\"? Cite a peer-reviewed source.", "answer": "Diabetes mellitus is a chronic metabolic disease characterized by abnormalities in insulin action, secretion, or both, which lead to persistent hyperglycemia. [ 1 , 2 ] Types 1 and 2 diabetes mellitus (T1DM and T2DM, respectively) are the 2 primary forms of the disease. [ 3 , 4 ] Although the pathophysiological causes and clinical manifestations of each type differ, all can result in serious complications if left untreated. [ 4 ] Dyslipidemia, a prevalent disorder in patients with diabetes, considerably increases the cardiovascular risk associated with the disease. Therefore, monitoring and managing lipid profiles is a crucial aspect of diabetes management. [ 5 , 6 ]\n\nIn T1DM, the immune system targets and destroys the pancreatic beta cells that produce insulin. [ 7 ] This results in a complete lack of insulin. [ 7 ] T1DM can occur at any age; however, it usually manifests in childhood or adolescence. To manage blood glucose levels, patients with T1DM need lifelong insulin therapy. [ 7 ] In patients with T1DM-associated dyslipidemia, low-density lipoprotein cholesterol (LDL-C), triglycerides, and total cholesterol levels are often elevated, while high-density lipoprotein cholesterol (HDL-C) levels are typically decreased. [ 8 , 9 ] These anomalies are worsened by poor glycemic management, which increases the risk of cardiovascular disease (CVD). [ 9 ]\n\nThe main risk factors for T2DM are insulin resistance, a condition in which the body’s cells lose their sensitivity to insulin, and a relative insulin deficit. [ 10 ] T2DM is closely associated with poor dietary habits, obesity, physical inactivity, and hereditary factors. [ 10 ] Although T2DM usually manifests in adulthood, it is becoming more common in younger populations. [ 11 ] In contrast to T1DM, T2DM is frequently managed with dietary changes, oral hypoglycemic medications, and, occasionally, insulin therapy. [ 12 ] Compared with T1DM, dyslipidemia in T2DM is usually more severe and manifests as an increase in small, dense LDL particles, decreased HDL-C levels, and increased triglyceride levels. [ 13 ] Patients with T2DM have an increased risk of CVD, largely attributable to this lipid profile, referred to as atherogenic dyslipidemia. [ 13 ]\n\nAlthough dyslipidemia is linked to both forms of diabetes, the patterns and underlying mechanisms differ. The main causes of lipid abnormalities in T1DM are inadequate insulin production and poor glycemic control. [ 8 ] On the other hand, central obesity, hypertension, and insulin resistance are major contributors to metabolic syndrome and T2DM-associated dyslipidemia. [ 13 ] With T2DM, the lipid profile is usually more atherogenic, which raises the risk of cardiovascular events. Understanding the distinctions in lipid profiles between T1DM and T2DM is essential for formulating customized treatment plans aimed at reducing the risk of CVD. A crucial component of comprehensive diabetes care involves managing dyslipidemia with medication, lifestyle changes, and optimal glycemic control. Further research into the mechanisms underlying these lipid abnormalities and their impact on cardiovascular outcomes will improve our capacity to properly monitor and treat diabetic dyslipidemia.\n\nDespite the extensive literature on dyslipidemia in diabetes, there is limited research specifically characterizing lipid profile variations between T1DM and T2DM in Saudi Arabia. Given the unique genetic, lifestyle and environmental factors affecting the Saudi population, understanding these differences is essential for preventive and therapeutic strategies. This study aims to bridge this gap by analyzing and comparing lipid profile patterns among Saudi patients with T1DM and T2DM, providing data that can enhance region-specific clinical management of dyslipidemia and cardiovascular risk in diabetic individuals.\n\n— Source (introduction, peer-reviewed): Fatemah Saleh Bin Saleh, Ahmed R. Alibrahim, Awad S. Alshahrani, et al. · (2025) · \"Lipid metabolism in type 1 and type 2 diabetes: A comparative cross-sectional study\" · Medicine · doi: 10.1097/MD.0000000000046758 · PMCID: PMC12747025 · PMID: 41465900\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-11824621-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC11824621", "pmid": "39638302", "doi": "10.3961/jpmph.24.424", "title": "Development and Validation of an Instrument to Assess the Safe Use of Antidiabetic Medication to Prevent Hypoglycemia Requiring Hospitalization Among Ambulatory Patients With Type 2 Diabetes Mellitus in Bali, Indonesia", "journal": "Journal of Preventive Medicine and Public Health", "publication_year": 2025, "citation": "Made Krisna Adi Jaya, Fita Rahmawati, Nanang Munif Yasin, et al. · (2025) · \"Development and Validation of an Instrument to Assess the Safe Use of Antidiabetic Medication to Prevent Hypoglycemia Requiring Hospitalization Among Ambulatory Patients With Type 2 Diabetes Mellitus in Bali, Indonesia\" · Journal of Preventive Medicine and Public Health · doi: 10.3961/jpmph.24.424 · PMCID: PMC11824621 · PMID: 39638302", "question": "What is the published background on \"Development and Validation of an Instrument to Assess the Safe Use of Antidiabetic Medication to Prevent Hypoglycemia Requiring…\"? Cite a peer-reviewed source.", "answer": "Patient safety is an essential aspect of healthcare services in various countries, including Indonesia. However, the implementation of comprehensive patient safety measures in Indonesian healthcare facilities remains challenging. This is primarily due to the lack of effective collaboration among health workers, managers, and support staff [ 1 , 2 ]. Previous studies have shown that hypoglycemia is a severe condition that is recognized as a leading cause of death. It is also associated with higher mortality rates, increased disease morbidity, and reduced quality of life, all of which significantly impact healthcare costs borne by both patients and the government [ 3 , 4 ].\n\nSeveral studies have indicated that the additional costs associated with hypoglycemia in patients with diabetes mellitus (DM) range from US$1353 to US$2285. In Indonesia, the government incurred total costs of US$23 million in 2016 for treating these cases [ 3 , 5 – 7 ]. Furthermore, the incidence of hypoglycemia among ambulatory DM patients resembles the iceberg phenomenon, with many cases remaining undetected and unreported within the health system. This issue may stem from patients’ limited knowledge and awareness of the condition. Approximately 90% of DM patients have reported experiencing mild to severe hypoglycemia while managing their condition with antidiabetic agents at home. A cohort study in Indonesia found that 99.4% of patients with type 2 diabetes mellitus (T2DM) experienced at least 1 hypoglycemic event over a 4-week period (prospective study), with a hypoglycemia incidence rate of 25.7 events per patient-year [ 8 – 10 ].\n\nIn line with these findings, clinical pharmacists play a crucial role in ensuring patient safety. These professionals are integral to drug services and are key in preventing adverse drug events [ 7 , 11 ]. Despite their significant role, clinical pharmacists still require guidance to effectively review medications. Currently, in Indonesia, there is no specific tool designed to assess the risk of hospitalization due to hypoglycemia caused by antihyperglycemic medications, highlighting a critical gap that needs to be addressed. Additionally, there is a local need for a simple and efficient method to evaluate the risk profile of T2DM patients experiencing ambulatory hypoglycemia, which can be conducted by clinical pharmacists. Consequently, this study aimed to develop an instrument for clinical pharmacists to assess the risk of medication-related hypoglycemia in ambulatory T2DM patients. The instrument, named “Medication-related Hypoglycemia Risk Score Assessment Tools (HYPOGLYRISK),” is expected to significantly enhance the quality of care and patient safety.\n\n— Source (introduction, peer-reviewed): Made Krisna Adi Jaya, Fita Rahmawati, Nanang Munif Yasin, et al. · (2025) · \"Development and Validation of an Instrument to Assess the Safe Use of Antidiabetic Medication to Prevent Hypoglycemia Requiring Hospitalization Among Ambulatory Patients With Type 2 Diabetes Mellitus in Bali, Indonesia\" · Journal of Preventive Medicine and Public Health · doi: 10.3961/jpmph.24.424 · PMCID: PMC11824621 · PMID: 39638302\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13071188-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC13071188", "pmid": "41810556", "doi": "10.1111/dom.70611", "title": "Acarbose or Canagliflozin vs. Placebo to Ameliorate Post‐Bariatric Hypoglycaemia: The Clinical Outcomes of the HypoBar I Randomised Clinical Trial", "journal": "Diabetes, Obesity & Metabolism", "publication_year": 2026, "citation": "Carolina B. Lobato, Clara Tornøe Winding, Kirstine N. Bojsen‐Møller, et al. · (2026) · \"Acarbose or Canagliflozin vs. Placebo to Ameliorate Post‐Bariatric Hypoglycaemia: The Clinical Outcomes of the HypoBar I Randomised Clinical Trial\" · Diabetes, Obesity & Metabolism · doi: 10.1111/dom.70611 · PMCID: PMC13071188 · PMID: 41810556", "question": "Summarize the abstract of the paper titled \"Acarbose or Canagliflozin vs. Placebo to Ameliorate Post‐Bariatric Hypoglycaemia: The Clinical Outcomes of the HypoBar I Randomised Clinical Trial\".", "answer": "Treatment options for post‐bariatric hypoglycaemia (PBH) are empirical. We aimed to investigate the efficacy and safety of acarbose and canagliflozin for the treatment of PBH.\n\nWe performed a randomised, double‐blinded, cross‐over, placebo‐controlled clinical trial where placebo, acarbose 50 mg thrice daily, and canagliflozin 300 mg twice daily were administered for 4 weeks. Treatment effects on blood glucose were monitored through blinded continuous glucose monitoring (CGM) for 10 days at the end of each intervention along with collection of patient‐reported outcomes. The primary outcome was the percentage of time below range during CGM (interstitial glucose below 3.9 mM/70 mg/dL).\n\nEleven participants with Roux‐en‐Y gastric bypass and documented PBH completed the trial. When compared with placebo, neither canagliflozin nor acarbose reduced the percentage of time below range (primary outcome, time below 3.9 mmol/L, median (IQR): screening 2.6 (0.7–5.1)%, placebo 1.2 (0.5–2.4)%, acarbose 1.1 (0.8–1.7)% and canagliflozin 0.8 (0.5–3.4)%). Both interventions, however, showed exploratory improvements in pre‐specified secondary outcomes, including time in range and glycaemic variability, as well as a reduction of symptoms of hypoglycaemia and frequency of symptomatic hypoglycaemic events, particularly with canagliflozin. Acarbose was associated with moderate and common side effects that caused treatment discontinuation in one participant. For both treatments, no severe adverse events were documented.\n\nHypoBar I is the first randomised, placebo‐controlled study of the treatment of PBH with acarbose or canagliflozin. Reduction in time below range was not achieved by either treatment; nevertheless, improvements in hypothesis‐generating secondary findings merit further investigation and validation. EudraCT number 2022‐000157‐87.\n\n— Source (abstract, peer-reviewed): Carolina B. Lobato, Clara Tornøe Winding, Kirstine N. Bojsen‐Møller, et al. · (2026) · \"Acarbose or Canagliflozin vs. Placebo to Ameliorate Post‐Bariatric Hypoglycaemia: The Clinical Outcomes of the HypoBar I Randomised Clinical Trial\" · Diabetes, Obesity & Metabolism · doi: 10.1111/dom.70611 · PMCID: PMC13071188 · PMID: 41810556\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12423126-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC12423126", "pmid": "40781566", "doi": "10.1007/s00125-025-06492-6", "title": "The impact of child type 1 diabetes on parental incomes in a welfare state context: quasi-experimental evidence from Swedish national registers", "journal": "Diabetologia", "publication_year": 2025, "citation": "Beatrice Kennedy, Mona-Lisa Wernroth, Sophie Langenskiöld, et al. · (2025) · \"The impact of child type 1 diabetes on parental incomes in a welfare state context: quasi-experimental evidence from Swedish national registers\" · Diabetologia · doi: 10.1007/s00125-025-06492-6 · PMCID: PMC12423126 · PMID: 40781566", "question": "What did the discussion section of the paper \"The impact of child type 1 diabetes on parental incomes in a welfare state context: quasi-experimental evidence from Swedish national registers\" cover?", "answer": "In this population-based study, parenting a child diagnosed with type 1 diabetes was linked to a sharp decline in work-related income. The decrease was more persistent in mothers and represented a larger proportion of their earnings than for fathers. In contrast, maternal pension-qualifying incomes increased after a child’s diabetes diagnosis, attributable to the parental care allowance. However, during the second half of the 17 year follow-up period, maternal pension-qualifying incomes gradually decreased and had not recovered by the end of the study period.\n\n— Source (discussion, peer-reviewed): Beatrice Kennedy, Mona-Lisa Wernroth, Sophie Langenskiöld, et al. · (2025) · \"The impact of child type 1 diabetes on parental incomes in a welfare state context: quasi-experimental evidence from Swedish national registers\" · Diabetologia · doi: 10.1007/s00125-025-06492-6 · PMCID: PMC12423126 · PMID: 40781566\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13158057-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC13158057", "pmid": "42125228", "doi": "10.3389/fendo.2026.1801546", "title": "Comparative predictive value of the cholesterol-high-density lipoprotein-glucose index versus the triglyceride-glucose index for gestational dysglycemia: a two-cohort study", "journal": "Frontiers in Endocrinology", "publication_year": 2026, "citation": "Mingliang Liu, Shihang Chen, Shi Wu, et al. · (2026) · \"Comparative predictive value of the cholesterol-high-density lipoprotein-glucose index versus the triglyceride-glucose index for gestational dysglycemia: a two-cohort study\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2026.1801546 · PMCID: PMC13158057 · PMID: 42125228", "question": "Summarize the abstract of the paper titled \"Comparative predictive value of the cholesterol-high-density lipoprotein-glucose index versus the triglyceride-glucose index for gestational dysglycemia: a two-cohort study\".", "answer": "Early risk stratification for gestational dysglycemia is important for improving maternal and neonatal outcomes. Derived from fasting triglycerides and glucose, the triglyceride–glucose (TyG) index is widely used to approximate insulin resistance, whereas the cholesterol-high-density lipoprotein-glucose (CHG) index incorporates broader lipid metabolism. We compared the associations and discriminative performance of TyG and CHG in a national survey discovery cohort and an independent clinical validation cohort.\n\nWe analyzed a survey-weighted discovery cohort from NHANES 2007–2018, in which the primary outcome was self-reported GDM history. We further evaluated an independent validation cohort with clinically diagnosed GDM (n = 217). Associations and predictive performance were assessed using multivariable logistic regression, receiver operating characteristic (ROC) analysis, calibration analysis, and decision curve analysis (DCA). Additional analyses included adjustment for continuous fasting blood glucose in NHANES, supportive analyses restricted to currently pregnant NHANES participants from 2007–2012 using proxy-defined gestational fasting dysglycemia (fasting blood glucose ≥5.1 mmol/L), and gestational-week-adjusted sensitivity analyses in the validation cohort.\n\nIn the NHANES discovery cohort, CHG showed a stronger association with self-reported GDM history than TyG in the primary adjusted models and yielded a numerically higher AUC than TyG. After additional adjustment for continuous fasting blood glucose, the association for TyG was attenuated, whereas CHG remained significantly associated. In the clinical validation cohort, CHG also showed numerically higher discriminative performance than TyG, and the overall findings remained directionally consistent after gestational-week adjustment. Supportive analyses in currently pregnant NHANES participants showed directionally similar but statistically imprecise estimates because of the limited sample size.\n\nBoth TyG and CHG are simple, low-cost indices associated with gestational dysglycemia/GDM. Across the discovery and validation cohorts, CHG generally showed stronger associations and numerically better discrimination than TyG; however, its overall discriminative performance remained modest and should be interpreted as that of a potential risk marker rather than a standalone clinical screening tool. Further prospective studies are needed to validate these findings.\n\n— Source (abstract, peer-reviewed): Mingliang Liu, Shihang Chen, Shi Wu, et al. · (2026) · \"Comparative predictive value of the cholesterol-high-density lipoprotein-glucose index versus the triglyceride-glucose index for gestational dysglycemia: a two-cohort study\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2026.1801546 · PMCID: PMC13158057 · PMID: 42125228\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-10910626-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC10910626", "pmid": "38418395", "doi": "10.1136/jitc-2023-008634", "title": "Fluctuations in plasma adrenocorticotropic hormone concentration may predict the onset of immune checkpoint inhibitor-related hypophysitis", "journal": "Journal for Immunotherapy of Cancer", "publication_year": 2024, "citation": "Hironori Bando, Masaaki Yamamoto, Shin Urai, et al. · (2024) · \"Fluctuations in plasma adrenocorticotropic hormone concentration may predict the onset of immune checkpoint inhibitor-related hypophysitis\" · Journal for Immunotherapy of Cancer · doi: 10.1136/jitc-2023-008634 · PMCID: PMC10910626 · PMID: 38418395", "question": "What is the published background on \"Fluctuations in plasma adrenocorticotropic hormone concentration may predict the onset of immune checkpoint inhibitor-related hypophysitis\"? Cite a peer-reviewed source.", "answer": "Immune checkpoint inhibitors (ICIs) are widely used to treat various malignant neoplasms. Programmed cell death protein 1 (PD-1), programmed death ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) are the ICI targets. However, ICI treatment can lead to immune-related adverse events (irAEs), including autoimmune endocrinopathies. Pituitary insufficiency due to ICI-related hypophysitis (ICI-RH) is a common irAE. The development of pituitary insufficiency in patients receiving ICIs is associated with better overall survival in several malignancies. 1 However, the appropriate diagnosis, early detection, and treatment of hypopituitarism are essential. Adrenal insufficiency due to hypopituitarism can be lethal if not properly managed. Life-threatening adrenal insufficiency is characterized by appetite loss, abdominal pain, and extreme fatigue, which mimics sepsis, brain metastasis, and cachexia. 2 The frequency and timing of onset vary with ICI class. The frequency of ICI-RH in anti-CTLA-4 antibody (Ab)-based regimens is 5%–10% with a median onset of 9–12 weeks, and that in anti-programmed cell death-1 (PD-1) and programmed cell death ligand 1 (PD-L1)-based regimens is <1% with a median onset of 26 weeks. 3 However, the timing of disease onset varies considerably among cases, hindering the prediction of disease onset.\n\nThe clinical features of anti-CTLA-4 and anti-PD-1/anti-PD-L1 Ab-RH differ. Anti-CTLA-4 Ab-RH causes panhypopituitarism, including secondary hypothyroidism, hypogonadotropic hypogonadism, and secondary adrenal insufficiency. 4 In contrast to anti-CTLA-4 Ab-RH, anti-PD-1/PD-L1 Ab-RH predominantly causes an isolated adrenocorticotropic hormone (ACTH) deficiency. 5 These different patterns may result from different underlying mechanisms. 6 However, secondary adrenal insufficiency accounts for 83% of ICI-RH cases. 7 Therefore, predictive markers for the onset of secondary adrenal insufficiency are essential.\n\nTahir et al reported autoantibodies against guanine nucleotide-binding protein G(olf) subunit alpha (GNAL) and integral membrane protein 2 B (ITM2B) as biomarkers for ICI-RH. 8 However, these biomarkers are still under investigation and cannot be measured routinely. Therefore, markers that can predict the onset of hypopituitarism under regular measures are necessary. Several studies have reported an elevation of the eosinophil fraction and count during the last visit and at the onset of hypopituitarism. 9 10 These studies raised a crucial point; however, one report also showed that the cortisol concentration had already mildly decreased at the last visit, which may be seen as a sign that ICI-RH is already under development. 9 Eosinophilia is a well-known marker of already developed adrenal insufficiency. 11\n\nThyroiditis is one of the most common irAEs. ICI-related thyroiditis typically occurs biphasically: thyrotoxicosis, followed by a subsequent persistent hypothyroidism. 12 In the initial thyrotoxicosis phase, free thyroxine and triiodothyronine levels are elevated while those of thyroid-stimulating hormone are suppressed. In the hypothyroidism phase, the pattern is reversed. The underlying mechanism of ICI-related thyroid dysfunction remains unknown. We speculated that, if the pituitary gland is damaged in ICI-RH by a mechanism similar to that of thyroiditis, plasma ACTH and serum cortisol levels, which are indicators of the hypothalamic pituitary adrenal (HPA) axis in routine practice, may fluctuate during the process. If so, they could potentially be used as predictive factors for the onset of secondary adrenal insufficiency in ICI-RH. To explore this possibility, we collected data on plasma ACTH and serum cortisol levels in patients using ICIs and analyzed fluctuations in hormone concentrations.\n\n— Source (introduction, peer-reviewed): Hironori Bando, Masaaki Yamamoto, Shin Urai, et al. · (2024) · \"Fluctuations in plasma adrenocorticotropic hormone concentration may predict the onset of immune checkpoint inhibitor-related hypophysitis\" · Journal for Immunotherapy of Cancer · doi: 10.1136/jitc-2023-008634 · PMCID: PMC10910626 · PMID: 38418395\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-10982440-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC10982440", "pmid": "37984965", "doi": "10.4235/agmr.23.0123", "title": "Prevalence of Adrenal Insufficiency in Korean Patients undergoing Total Knee Arthroplasty", "journal": "Annals of Geriatric Medicine and Research", "publication_year": 2023, "citation": "So Won Baek, Jung Ho Noh, Yeon Sik Heo · (2023) · \"Prevalence of Adrenal Insufficiency in Korean Patients undergoing Total Knee Arthroplasty\" · Annals of Geriatric Medicine and Research · doi: 10.4235/agmr.23.0123 · PMCID: PMC10982440 · PMID: 37984965", "question": "Summarize the abstract of the paper titled \"Prevalence of Adrenal Insufficiency in Korean Patients undergoing Total Knee Arthroplasty\".", "answer": "This study investigated the prevalence of adrenal insufficiency among patients admitted for total knee arthroplasty (TKA) due to osteoarthritis and identified factors contributing to adrenal insufficiency.\n\nWe divided the patients into two groups based on the results of preoperative standard-dose short synchronous stimulation tests: group 1 (adrenal insufficiency) and group 2 (normal adrenal function). We also assessed the prevalence of adrenal insufficiency and compared the numbers of patients who received oral steroids, the frequency of previous steroid injection use, and the frequency of systemic symptoms of steroid depletion such as fatigue and loss of appetite between the two groups. Multiple regression analysis was performed to identify factors related to adrenal insufficiency.\n\nThe prevalence of adrenal insufficiency was 60.0% (120/200). Group 1 had higher numbers of previous steroid injections (12.8±10.2 vs. 6.8±7.9) and patients taking oral steroids (18/120 vs. 3/80) (p<0.001 and p=0.011, respectively). The frequency of systemic symptoms of steroid depletion, such as fatigue and loss of appetite, was also higher in group 1 (94/120 vs. 42/80, p<0.001). Recent steroid injections and loss of appetite were associated with adrenal insufficiency (p=0.002 and p=0.009, respectively).\n\nThe results of this study revealed a high prevalence of adrenal insufficiency in Korean patients hospitalized for TKA due to end-stage osteoarthritis. Recent steroid injections were causally related to the development of adrenal insufficiency. Therefore, adrenal function should be assessed preoperatively to prevent postoperative complications related to adrenal insufficiency.\n\n— Source (abstract, peer-reviewed): So Won Baek, Jung Ho Noh, Yeon Sik Heo · (2023) · \"Prevalence of Adrenal Insufficiency in Korean Patients undergoing Total Knee Arthroplasty\" · Annals of Geriatric Medicine and Research · doi: 10.4235/agmr.23.0123 · PMCID: PMC10982440 · PMID: 37984965\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12982865-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC12982865", "pmid": "41836627", "doi": "10.1177/20552076261425402", "title": "Digital health technologies and stakeholder incentives in type-2 diabetes prevention", "journal": "Digital Health", "publication_year": 2026, "citation": "Wasu Mekniran, Wilma Diethelm, Victoire Stalder, et al. · (2026) · \"Digital health technologies and stakeholder incentives in type-2 diabetes prevention\" · Digital Health · doi: 10.1177/20552076261425402 · PMCID: PMC12982865 · PMID: 41836627", "question": "What did the discussion section of the paper \"Digital health technologies and stakeholder incentives in type-2 diabetes prevention\" cover?", "answer": "Despite well-established scientific evidence for the prevention of T2D through sustained lifestyle change, 2 – 5 preventive programs are seldom integrated and sustained within traditional healthcare systems. How is the uptake and systemic implementation of prevention associated with stakeholder incentives, specifically between individuals, payers, and providers? Grounded in an ecosystem theory 8 , 34 and the e3-value ontology, 36 , 37 this is the first study, to our knowledge, that examines incentives among individuals, payers, and providers and the associations between DHT adoption and stakeholder value flows in the digital T2D prevention context.\n\nOur findings support theoretical perspectives that prevention is contingent on a dynamic network of interdependent actors. 33 , 34 We identify three main insights. First, financial and non-financial incentives for lifestyle-based prevention are often temporally misaligned: engagement in lifestyle-based prevention may provide individuals with short-term benefits such as convenience, rewards, and improved health benefits, while payers are often motivated to support prevention programs as a function of long-term cost savings. Second, we find that DHT adoption for T2D prevention is associated with three main incentive patterns: personalization and convenience for individuals, value-based payment models for payers, and improving workflow efficiency for providers. DHTs may help support the realignment of stakeholder incentives through three key interrelated mechanisms: (i) sustaining individual engagement in prevention programs through personalized micro-incentives, (ii) supporting value-based payment models for payers, and (iii) automating workflows for providers. Using the e3-value framework, we visualize these reconfigured value exchanges ( Figure 2 ), illustrating how DHTs may support a shared data-driven infrastructure to enhance individual engagement, performance tracking, and shared accountability across the ecosystem. 28\n\nBuilding on the stakeholder incentive literature, 10 , 13 our identification of varying financial and non-financial is consistent with perspectives that prevention incentives remain highly fragmented across stakeholder groups As detailed in Table 4 , this fragmentation is particularly evident in the temporal dimension: individuals are primarily motivated to engage in lifestyle programs and prevention efforts based on short-term, tangible rewards such as cashback, gamified tokens, or convenience-enhancing lifestyle tracking apps (i.e., “Upload [photos of] your meals for today. You earn a few utility tokens,” ID 23), In contrast, insurers and providers are more likely to prioritize delayed benefits like reduced readmissions or loyalty-based retention to their services and plans over extended periods of time, and at the population level (Prior work examining incentives has specifically focused on provider reimbursement models and patient adherence to treatment plans, finding fragmented financial incentives among various healthcare stakeholders (i.e., pay-for-service models disincentivizing preventive care). 17\n\nHere, we also identified perceived trust in data fairness as an additional non-financial incentive for individuals to engage with DHTs for T2D prevention. This finding reframes data privacy, not as a compliance issue, 70 but as a potential behavioral motivator, potentially associated with willingness to engage with DHTs. For providers and payers, data privacy primarily functions as a regulatory compliance incentive, crucial for avoiding penalties and maintaining public trust. Furthermore, strong data privacy can also serve as a non-financial incentive for patient and customer acquisition or retention.\n\n— Source (discussion, peer-reviewed): Wasu Mekniran, Wilma Diethelm, Victoire Stalder, et al. · (2026) · \"Digital health technologies and stakeholder incentives in type-2 diabetes prevention\" · Digital Health · doi: 10.1177/20552076261425402 · PMCID: PMC12982865 · PMID: 41836627\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-9875820-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC9875820", "pmid": "36695783", "doi": "10.14814/phy2.15577", "title": "How dietary amino acids and high protein diets influence insulin secretion", "journal": "Physiological Reports", "publication_year": 2023, "citation": "Yuuki Yanagisawa · (2023) · \"How dietary amino acids and high protein diets influence insulin secretion\" · Physiological Reports · doi: 10.14814/phy2.15577 · PMCID: PMC9875820 · PMID: 36695783", "question": "What is the published background on \"How dietary amino acids and high protein diets influence insulin secretion\"? Cite a peer-reviewed source.", "answer": "Glucose is the simplest and most abundant monosaccharide known to man and is the primary biological fuel source for the human body (Hantzidiamantis & Lappin, 2022 ). Glucose is obtained from three fundamental sources—exogenously from dietary intake, from glycogenolysis in the liver and muscle, and gluconeogenesis in the liver, kidneys, and intestine (Aronoff et al., 2004 ).\n\nGlucose homeostasis is the maintenance and regulation of blood glucose levels within the narrow range of 4 to 6 mmol/L and is critical for maintaining the normal physiological functioning of most organs and tissues (Pozo, 2018 ; Roder et al., 2016 ). Glucose homeostasis is achieved through the coordination of glucose sensing mechanisms which detect fluctuations in blood glucose concentration with multiple effector responses which act to re‐establish blood glucose levels within this tight target range (Pozo, 2018 ). Effector responses are mediated by several complex neural and endocrine networks, involving several neurotransmitters, neuropeptides, and glucoregulatory hormones (Aronoff et al., 2004 ). The pancreas is a critical source of glucoregulatory hormones, which are synthesized and secreted by collections of specialized endocrine cells found within the islets of Langerhans (Aronoff et al., 2004 ; Petersen, 2018 ; Roder et al., 2016 ). Insulin is an anabolic hormone secreted by pancreatic β cells in response to increased blood glucose concentration (Petersen, 2018 ). Insulin decreases blood glucose concentrations by promoting glucose uptake into muscle and adipose tissues, stimulating hepatic glycogenesis, and downregulating gluconeogenesis (Aronoff et al., 2004 ; Petersen, 2018 ). Insulin also increases cellular uptake of amino acids from the peripheral circulation, facilitating intracellular protein synthesis (Zakaria et al., 2021 ). In contrast, glucagon is released from α cells in states of fasting and hypoglycemia. Glucagon raises blood glucose concentration by inducing gluconeogenesis and glycogenolysis (Roder et al., 2016 ).\n\nIn addition to insulin and glucagon, several other glucoregulatory hormones contribute to glucose homeostasis (Aronoff et al., 2004 ; Renner et al., 2015 ). These include somatostatin, and the incretins glucagon‐like peptide 1 (GLP‐1) and glucose‐dependent insulinotropic peptide (GIP). Somatostatin is secreted from delta cells within the islets of Langerhans, stomach, and small intestine (O'Toole & Sharma, 2022 ). Somatostatin inhibits the release of both insulin and glucagon, as well as the release of pancreatic exocrine secretions (O'Toole & Sharma, 2022 ; Strowski et al., 2000 ). In comparison, the latter two peptide hormones GLP‐1 and GIP are secreted from L‐ and K‐enteroendocrine cells of the intestine, respectively (Aronoff et al., 2004 ). Both GLP‐1 and GIP potentiate glucose‐dependent insulin secretion, enhance β‐cell proliferation, and downregulate β‐cell apoptosis, and GLP‐1 also inhibits glucagon secretion (Renner et al., 2015 ).\n\nChronic impairment or deficiency of these glucoregulatory responses can lead to the development of diabetes mellitus, a major global health epidemic associated with considerable clinical sequelae, and vast financial and healthcare ramifications (O'Connell & Manson, 2019 ). At present, 463 million people worldwide are estimated to suffer from diabetes mellitus, which can be classified as Type 1 or Type 2 diabetes mellitus (T1DM or T2DM) (Saeedi et al., 2019 ). In the UK, approximately 90% of the diabetic population have T2DM, with T1DM accounting for 8% of patients (Diabetes UK, n.d. ). T2DM is characterized by peripheral resistance to insulin coupled with progressive β‐cell failure and relative insulin deficiency (Strowski et al., 2000 ). In contrast, T1DM is defined by complete or near complete insulin deficiency due to the autoimmune destruction of β cells (Diabetes UK, n.d. ).\n\nGiven the long‐term complications of T2DM such as cardiovascular and cerebrovascular disease, congestive heart failure, and predisposition to recurrent infection, an ever‐growing demand exists to better understand and improve persistent hyperglycemia associated with T2DM, potentially through the use of high protein diets (HPDs) (Diabetes UK, n.d. ; Toft‐Nielsen et al., 2001 ).\n\nA HPD is specifically defined as a diet supplying 35% or more of daily total energy intake in the form of protein (O'Connell & Manson, 2019 ; Saeedi et al., 2019 ). Proteins are macronutrients, composed of one or more chains of different amino acids. Animal proteins such as whey, casein, egg, fish, beef, and chicken, along with plant‐based proteins including soy, pea, brown rice, and chickpea are essential for multiple physiological and homeostatic activities within the body (Lupton et al., 2005 ). In particular, amino acids and HPDs can also influence glucose homeostasis (Galbreath et al., 2018 ; Lupton et al., 2005 ; Morell, 2017 ; Parker et al., 2002 ; Pasiakos et al., 2013 ; Stokes et al., 2018 ; Tipton, 2011 ). Multiple studies conducted in rodents and humans have shown that consumption of protein and amino acids leads to weight loss and improves glucose homeostasis (Galbreath et al., 2018 ; Morell, 2017 ; Parker et al., 2002 ; Pasiakos et al., 2013 ; Stokes et al., 2018 ). Although the effects of HPDs are generated by the physiological activities of their constituent amino acids, pharmacological administration of amino acids can differentially impact glucose homeostasis. This is in part due to differences in digestion time, the rate of gastric emptying and release into the blood stream, and the utilization following digestion (Pena et al., 2015 ).\n\nDespite the physiological benefits of amino acids and HPDs, there are concerns regarding the implications of their long‐term consumption, particularly nephrotoxicity (Cirillo et al., 2014 ; Knight et al., 2003 ; Pasiakos et al., 2013 ). Several long‐term observational studies conducted in adults have found an association between high protein intake and decline in renal function, in both participants with normal renal function and those with pre‐existing renal disease (Cirillo et al., 2014 ; Knight et al., 2003 ). These complications, along with relatively poor levels of adherence to HPDs, have raised the question if the mechanisms by which amino acids and HPDs improve glucose homeostasis can be exploited without the need for the consumption of high levels of dietary protein.\n\nThis review will examine the different insulinotropic and non‐insulinotropic mechanisms by which amino acids and HPDs influence glucose homeostasis and their supporting evidence. The translational potential to exploit these mechanisms for the management of diabetes mellitus will also be discussed.\n\n— Source (introduction, peer-reviewed): Yuuki Yanagisawa · (2023) · \"How dietary amino acids and high protein diets influence insulin secretion\" · Physiological Reports · doi: 10.14814/phy2.15577 · PMCID: PMC9875820 · PMID: 36695783\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-8622801-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC8622801", "pmid": "34836158", "doi": "10.3390/nu13113903", "title": "Low-Carbohydrate Diet among Children with Type 1 Diabetes: A Multi-Center Study", "journal": "Nutrients", "publication_year": 2021, "citation": "Vit Neuman, Lukas Plachy, Stepanka Pruhova, et al. · (2021) · \"Low-Carbohydrate Diet among Children with Type 1 Diabetes: A Multi-Center Study\" · Nutrients · doi: 10.3390/nu13113903 · PMCID: PMC8622801 · PMID: 34836158", "question": "Summarize the abstract of the paper titled \"Low-Carbohydrate Diet among Children with Type 1 Diabetes: A Multi-Center Study\".", "answer": "Aims/hypothesis: The proportion of children with type 1 diabetes (T1D) who have experience with low-carbohydrate diet (LCD) is unknown. Our goal was to map the frequency of LCD among children with T1D and to describe their clinical and laboratory data. Methods: Caregivers of 1040 children with T1D from three centers were addressed with a structured questionnaire regarding the children’s carbohydrate intake and experience with LCD (daily energy intake from carbohydrates below 26% of age-recommended values). The subjects currently on LCD were compared to a group of non-LCD respondents matched to age, T1D duration, sex, type and center of treatment. Results: A total of 624/1040 (60%) of the subjects completed the survey. A total of 242/624 (39%) subjects reported experience with voluntary carbohydrate restriction with 36/624 (5.8%) subjects currently following the LCD. The LCD group had similar HbA1c (45 vs. 49.5, p = 0.11), lower average glycemia (7.0 vs. 7.9, p = 0.02), higher time in range (74 vs. 67%, p = 0.02), lower time in hyperglycemia >10 mmol/L (17 vs. 20%, p = 0.04), tendency to more time in hypoglycemia <3.9 mmol/L(8 vs. 5%, p = 0.05) and lower systolic blood pressure percentile (43 vs. 74, p = 0.03). The groups did not differ in their lipid profile nor in current body height, weight or BMI. The LCD was mostly initiated by the parents or the subjects themselves and only 39% of the families consulted their decision with the diabetologist. Conclusions/interpretation: Low carbohydrate diet is not scarce in children with T1D and is associated with modestly better disease control. At the same time, caution should be applied as it showed a tendency toward more frequent hypoglycemia.\n\n— Source (abstract, peer-reviewed): Vit Neuman, Lukas Plachy, Stepanka Pruhova, et al. · (2021) · \"Low-Carbohydrate Diet among Children with Type 1 Diabetes: A Multi-Center Study\" · Nutrients · doi: 10.3390/nu13113903 · PMCID: PMC8622801 · PMID: 34836158\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12678572-conclusion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-conclusion", "source": "PubMed Central open-access full text", "pmcid": "PMC12678572", "pmid": "40866742", "doi": "10.1007/s42000-025-00712-9", "title": "Glucose dynamics in glycogen storage disease type IXa with novel PHKA2 variants: insights from our experience and a comprehensive review of the disease spectrum", "journal": "Hormones (Athens, Greece)", "publication_year": 2025, "citation": "Federico Baronio, Giacomo Biasucci, Egidio Candela, et al. · (2025) · \"Glucose dynamics in glycogen storage disease type IXa with novel PHKA2 variants: insights from our experience and a comprehensive review of the disease spectrum\" · Hormones (Athens, Greece) · doi: 10.1007/s42000-025-00712-9 · PMCID: PMC12678572 · PMID: 40866742", "question": "What does the published research conclude about \"Glucose dynamics in glycogen storage disease type IXa with novel PHKA2 variants: insights from our experience and a comprehensive review of…\"? Cite a peer-reviewed source.", "answer": "Our clinical cases have shown that patients with GSX IXa present only with hypoglycemia without any liver abnormalities or other significant symptoms. Therefore, if a patient experiences recurrent episodes of ketotic hypoglycemia and other endocrinological causes that have been ruled out, it is crucial to consider genetic testing for GSX IXa. A timely diagnosis can help establish an appropriate diet plan and prevent complications.\n\n— Source (conclusions, peer-reviewed): Federico Baronio, Giacomo Biasucci, Egidio Candela, et al. · (2025) · \"Glucose dynamics in glycogen storage disease type IXa with novel PHKA2 variants: insights from our experience and a comprehensive review of the disease spectrum\" · Hormones (Athens, Greece) · doi: 10.1007/s42000-025-00712-9 · PMCID: PMC12678572 · PMID: 40866742\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12226158-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC12226158", "pmid": "40612706", "doi": "10.1155/pedi/8425032", "title": "Hypertriglyceridemia in New-Onset Type 1 Pediatric Diabetes", "journal": "Pediatric Diabetes", "publication_year": 2025, "citation": "Colleen A. Macke, Iman Al-Gadi, Nidhi Bansal, et al. · (2025) · \"Hypertriglyceridemia in New-Onset Type 1 Pediatric Diabetes\" · Pediatric Diabetes · doi: 10.1155/pedi/8425032 · PMCID: PMC12226158 · PMID: 40612706", "question": "Summarize the abstract of the paper titled \"Hypertriglyceridemia in New-Onset Type 1 Pediatric Diabetes\".", "answer": "Hypertriglyceridemia (HTG) in the setting of newly diagnosed diabetes is common in both adult and pediatric populations, as insulin deficiency promotes lipolysis and impairs triglyceride (TG) clearance. Severe HTG (defined as TG levels above 1000 mg/dL) in pediatric patients with new-onset type 1 diabetes mellitus (T1D) is rare; the true incidence and sequela of this phenomenon have not been well characterized. We present a single-center experience on severe HTG in pediatric patients with new-onset T1D between 2013 and 2022 and summarize the cases previously reported in the literature. Our cases display variability in their presentation and in their association with high-risk complications, such as acute pancreatitis. We discuss suggestions of early screening for HTG and pancreatitis in patients with protracted abdominal pain, and close monitoring of those identified to have significant HTG.\n\n— Source (abstract, peer-reviewed): Colleen A. Macke, Iman Al-Gadi, Nidhi Bansal, et al. · (2025) · \"Hypertriglyceridemia in New-Onset Type 1 Pediatric Diabetes\" · Pediatric Diabetes · doi: 10.1155/pedi/8425032 · PMCID: PMC12226158 · PMID: 40612706\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-11269257-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC11269257", "pmid": "39055981", "doi": "10.3389/fcimb.2024.1421128", "title": "Association between gut microbiota and adrenal disease: a two-sample Mendelian randomized study", "journal": "Frontiers in Cellular and Infection Microbiology", "publication_year": 2024, "citation": "Yue-Yang Zhang, Yao-Wen Liu, Bing-Xue Chen, et al. · (2024) · \"Association between gut microbiota and adrenal disease: a two-sample Mendelian randomized study\" · Frontiers in Cellular and Infection Microbiology · doi: 10.3389/fcimb.2024.1421128 · PMCID: PMC11269257 · PMID: 39055981", "question": "What is the published background on \"Association between gut microbiota and adrenal disease: a two-sample Mendelian randomized study\"? Cite a peer-reviewed source.", "answer": "Adrenal diseases are vital components of endocrine system disorders, chiefly encompassing Adrenocortical insufficiency (AI), Cushing syndrome(CS), and Hyperaldosteronism(HA) ( Salman and Cohen, 2021 ). AI manifests as adrenal cortex dysfunction, resulting in absolute or relative insufficiency of cortisol secretion ( Bancos et al., 2015 ). Primary adrenal insufficiency, such as Addison’s disease, is relatively rare and typically arises from direct adrenal failure ( Erichsen et al., 2009 ; Ross and Levitt, 2013 ; Bornstein et al., 2016 ). Conversely, secondary adrenal cortex insufficiency, more prevalent, stems mainly from pituitary damage affecting adrenocortical hormone secretion ( Grossman, 2010 ; Hahner et al., 2021 ). AI frequently progresses to adrenal crisis, significantly heightening patient mortality rates ( Dineen et al., 2019 ). Prolonged elevation of endogenous cortisol levels can result in Cushing’s syndrome, leading to numerous organ complications such as hypertension, obesity, dysregulation of glucose and lipid metabolism, and cognitive impairment ( Pivonello et al., 2016 ). These complications arise due to the impact on the nervous and immune systems, ultimately diminishing the patient’s quality of life ( Hatipoglu, 2012 ; Ferriere and Tabarin, 2020 ). Hyperaldosteronism primarily involves primary aldosterone elevation and stands as a frequent cause of hypertension, often inflicting direct damage on target organs ( Zennaro et al., 2020 ). Compared to diabetes, the incidence of adrenal diseases is relatively lower. However, with advancements in medical technology, their global incidence is on the rise. The prevalence of CS is 39.1 per million, with an annual incidence of 2.4 per 100,000. Reports indicate that since 1974, the prevalence of CS has increased almost linearly ( Steffensen et al., 2010 ), while the prevalence of AI has reached 100-140 per million ( Hahner et al., 2021 ). HS most commonly manifests as hypertension, and it is estimated that approximately 6%-10% of hypertensive patients are affected by HS ( Monticone et al., 2017 ). These data suggest that adrenal diseases are impacting an increasing number of patients, gradually becoming a significant focus of global public health efforts.\n\nThe gut microbiota, defined as the microbial community residing in the human gastrointestinal tract, has garnered increasing attention due to mounting evidence suggesting its close association with various diseases in the body. For example, a case-control study observed a reduction in Bacteroidetes and an increase in Firmicutes and Proteobacteria in patients with CS ( Zhang et al., 2022 ). In a study involving 54 psoriasis patients and 27 healthy controls, genetic material from gut bacteria was detected in the plasma of 16 psoriasis patients, but not in any healthy controls. This discrepancy may be attributed to a reduction in the abundance of potential probiotics in psoriasis patients, resulting in immune system imbalance ( Mahmud et al ). Moreover, the relationship between obesity and gut microbiota is well established ( Gomes et al., 2018 ). It is widely believed that gut microbiota dysbiosis primarily induces disease by influencing the gut-brain axis and regulating brain function ( Anand et al., 2022 ). Animal studies have shown that microbial colonization in mice affects the development of the hypothalamic-pituitary-adrenal axis postnatally, suggesting that gut microbiota significantly impact adrenal function ( Sudo et al., 2004 ). Another study found that the excessive release of lipopolysaccharides into the blood by Gram-negative bacteria can hyperactivate the hypothalamic-pituitary-adrenal axis, inducing systemic and neuroinflammation, leading to increased cortisol secretion and severely disrupting central nervous system homeostasis ( Moylan et al., 2014 ). The probiotic B. pseudocatenulatum (CECT 7765) has been shown to reverse abnormal stress responses caused by dysregulation of glucocorticoid receptors ( Agusti et al., 2018 ). Treatment with Lactobacillus sp. during early maternal separation stress can normalize hypothalamic-pituitary-adrenal axis activity ( Gareau et al., 2007 ). L. farciminis has also been found to prevent excessive activation of the hypothalamic-pituitary-adrenal axis caused by restraint stress ( Ait-Belgnaoui et al., 2012 ).However, due to challenges in confirming exposure and outcome times in case-control studies, and because similar observational studies draw conclusions based on changes in microbial composition in patients’ feces, they are susceptible to various confounding factors such as age and environment ( Rinninella et al., 2019 ). These limitations impede causal inferences between gut microbiota and adrenal diseases, leaving the causal relationship between gut microbiota and adrenal diseases unresolved.\n\nMendelian randomization(MR) is currently recognized as a method capable of inferring causality between exposure and outcome. It utilizes genetic variants associated with exposure as instrumental variables to assess the association between exposure and outcome ( Greenland, 2000 ; Emdin et al., 2017 ). According to Mendelian genetic laws, genetic information is randomly allocated at conception, occurring prior to the onset of any disease. This randomization significantly minimizes the influence of environmental and lifestyle confounding factors. MR has been widely utilized to explore causal relationships between gut microbiota and various diseases, including preeclampsia ( Li et al., 2022 ), autoimmune diseases ( Xu et al., 2021 ), and others. However, research on the relationship between gut microbiota and AI, CS, and HA is relatively scarce. Thus, this study aimed to investigate the causal relationship between gut microbiota and various adrenal diseases by conducting a comprehensive two-sample MR analysis on three adrenal diseases, namely AI, CS, and HA.\n\n— Source (introduction, peer-reviewed): Yue-Yang Zhang, Yao-Wen Liu, Bing-Xue Chen, et al. · (2024) · \"Association between gut microbiota and adrenal disease: a two-sample Mendelian randomized study\" · Frontiers in Cellular and Infection Microbiology · doi: 10.3389/fcimb.2024.1421128 · PMCID: PMC11269257 · PMID: 39055981\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13034286-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC13034286", "pmid": "41887636", "doi": "10.1136/bmjopen-2025-111570", "title": "Lived experiences of children with type 1 diabetes mellitus and their parents: a qualitative descriptive study from eastern India", "journal": "BMJ Open", "publication_year": 2026, "citation": "K Jayakrishnan, Poonam Joshi, Aparajita Guin, et al. · (2026) · \"Lived experiences of children with type 1 diabetes mellitus and their parents: a qualitative descriptive study from eastern India\" · BMJ Open · doi: 10.1136/bmjopen-2025-111570 · PMCID: PMC13034286 · PMID: 41887636", "question": "What is the published background on \"Lived experiences of children with type 1 diabetes mellitus and their parents: a qualitative descriptive study from eastern India\"? Cite a peer-reviewed source.", "answer": "Type 1 diabetes mellitus (T1DM) in children under 20-year old is a chronic autoimmune disease where the body’s immune system mistakenly attacks and destroys insulin-producing cells in the pancreas. 1 This destruction leads to a deficiency in insulin, a hormone essential for regulating blood sugar levels, resulting in various short-term and long-term health complications. 2 In 2022, there were an estimated 8.75 million people globally living with T1DM, with a 95% uncertainty interval ranging from 8.4 to 9.1 million. Approximately one-fifth, or 1.9 million, of these individuals were from low-income and lower middle-income countries. 3\n\nIatrogenic hypoglycaemia is an inevitable aspect of life for individuals with T1DM. These individuals experience numerous episodes of asymptomatic hypoglycaemia. For instance, a study using subcutaneous glucose sensors in people with T1DM found that their glucose levels were at or below 70 mg/dL (3.9 mmol/L) for an average of 1.5 hours each day, which constitutes 6.3% of the time. 4 Severe hypoglycaemia in children with type 1 diabetes is marked by cognitive dysfunctions like convulsions and coma that require external help and can be fatal, causing 4%–10% of deaths of the hypoglycaemic children. 5 Children with type 1 diabetes, along with their families, are at risk of heightened anxiety, insufficient sleep and a reduced quality of life. Particularly for families with younger children, the fear of severe hypoglycaemia during the night is a major concern. 6 This fear may drive them to accept higher blood glucose levels and engage in behaviours that avoid hypoglycaemia, ultimately resulting in suboptimal glycaemic control. 57 9\n\nWitnessing severe hypoglycaemia events, such as seizures or loss of consciousness, can cause lasting distress, even if the child does not remember the episode. The fear of hypoglycaemia reduces the quality of life for both parents and children, significantly affecting parents’ emotional well-being and daily life. Addressing these psychological issues is crucial for effective diabetes management, necessitating education, coping strategies and emotional support. 10 12\n\nManaging a child’s chronic illness adds to the burden, with parents struggling with the technical aspects of blood glucose management and balancing these responsibilities with other obligations. This role disrupts family dynamics and places emotional burdens on parents, who must adapt as their child grows and takes on more responsibility. 13 14 Financial strain and lack of social support further exacerbate these challenges. Recognising and addressing these issues is essential for healthcare providers to support both the child with T1DM and their parents. 15 According to a cross-sectional survey from North India, families spend an average of ₹55 185 annually on diabetes care, with insulin and glucose monitoring alone accounting for more than 90% of direct medical costs. Alarmingly, over 30% of families spend more than half their income on T1DM-related expenses. 16 Similarly, a study from a government-funded hospital in Uttar Pradesh found that the average annual cost per child was ₹27 915, with 87% of costs paid out-of-pocket and insulin and glucose testing supplies comprising nearly 80% of expenses. 17 Continuous Glucose Monitors (CGMs) and flash glucose monitoring systems remain largely inaccessible to most families due to their high upfront and maintenance costs and the lack of government subsidies. While some families with higher socioeconomic status or employer insurance may afford such devices, their widespread adoption in lower income settings remains extremely limited, highlighting the need for policy-level interventions to improve access and affordability. 16\n\nShortly after diagnosis, parents often experience shock, sadness, anxiety, disbelief, fear, frustration and despair. 8 14 15 18 19 Uncertainty about the disease’s progression and social impact can trigger guilt and anxiety, exacerbated by the condition’s ‘invisibility’ before diagnosis. 20 Following a child’s hospital discharge, caregivers frequently report worry, anxiety, sadness, stigma, annoyance and guilt, intensified by uncertainty about disease progression. 1 Healthcare providers must address these issues to offer holistic support, helping caregivers manage their mental health while caring for a child with T1DM. 11 12\n\nThis study is necessary to comprehensively understand the multifaceted difficulties encountered by both children with T1DM and their parents in eastern India. To the best of our knowledge, there are no qualitative studies from India that explore the lived experiences of both children with T1DM and their parents. By exploring the experiences and perspectives of both parents and children, the study aims to identify specific challenges in managing T1DM and understand the psychological, emotional and practical implications of the disease. The objectives of this study are to explore the challenges faced by parents in managing their children’s condition and to delve into the challenges experienced by the children themselves.\n\n— Source (introduction, peer-reviewed): K Jayakrishnan, Poonam Joshi, Aparajita Guin, et al. · (2026) · \"Lived experiences of children with type 1 diabetes mellitus and their parents: a qualitative descriptive study from eastern India\" · BMJ Open · doi: 10.1136/bmjopen-2025-111570 · PMCID: PMC13034286 · PMID: 41887636\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-10675710-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC10675710", "pmid": "38004112", "doi": "10.3390/nu15224717", "title": "The Impact of Maternal Plant-Based Diet on Obstetric and Neonatal Outcomes—A Cross-Sectional Study", "journal": "Nutrients", "publication_year": 2023, "citation": "Paulina Przybysz, Adrian Kruszewski, Joanna Kacperczyk-Bartnik, et al. · (2023) · \"The Impact of Maternal Plant-Based Diet on Obstetric and Neonatal Outcomes—A Cross-Sectional Study\" · Nutrients · doi: 10.3390/nu15224717 · PMCID: PMC10675710 · PMID: 38004112", "question": "What did the discussion section of the paper \"The Impact of Maternal Plant-Based Diet on Obstetric and Neonatal Outcomes—A Cross-Sectional Study\" cover?", "answer": "In this study, a plant-based diet was relatively common among pregnant women, with 5.7% of them being vegetarian and 2.5% being fully vegan based on reported dietary habits. The results showed that a plant-based diet—both during the preconception period and during pregnancy—was not associated with the incidence of anemia during pregnancy and gestational hypertension in univariate analysis. Multivariate analysis showed that prepregnancy BMI was a contributing factor to gestational hypertension incidence in the plant-based diet group, though the numbers are small. Additionally, a meat-free diet during the preconception period did not change the risk of developing GDM but during pregnancy was associated with a lower incidence of GDM. The GDM risk increased with the prepregnancy BMI increase in the omnivore group. There were fewer overweight women in the plant-based group than in the omnivore group, and the incidence of GDM was also affected by prepregnancy BMI, as shown by multivariate analysis.\n\nThe mechanism of plant-based-diet action on organisms is various. This diet has a beneficial effect on the microbiome by inducing the development of more diverse and stable microbial systems, hence supporting overall health [ 20 ]. The literature indicates that vegetarianism can increase nitric oxide bioavailability and decrease reactive oxygen species [ 6 ]. The semiquantitative review conducted by Jaworsky et al. of women with high risk for GDM pointed out that a plant-based diet and phytochemicals may reduce blood glucose and improve antioxidant activity to reduce the oxidative stress that is often associated with GDM [ 21 ]. Also, plant-rich meals significantly increase the serum levels of glucagon-like peptide-1 (GLP-1), a hormone that augments the secretion of insulin [ 6 ]. In our paper, we focused on the impact of diet on chosen maternal and neonatal outcomes, but further studies examining the impact and its mechanisms are needed.\n\nThe research by Yisahak et al. included 1948 low-risk pregnant women of four races in the USA, and the results showed that vegetarianism did not exhibit associations with maternal outcomes including GDM, hypertensive disorders, and anemia [ 22 ]. There is evidence that a higher intake of red and processed meat is a risk factor for developing GDM [ 23 ] and type 2 diabetes mellitus [ 24 , 25 ].\n\nThe study conducted by Carter et al. revealed that a vegan diet (low in arachidonic acid) might provide protection against preeclampsia and could alleviate most if not all of the signs and symptoms of preeclampsia [ 26 ]. Research performed by Pistollato et al. suggests that maternal nutritional patterns characterized by a low intake of plant-derived foods could increase the risk of gestation-related issues, such as preeclampsia and pregravid obesity, and contribute to the onset of pediatric diseases [ 27 ].\n\nThe result of our research showed that physical activity over 90 min a week is associated with a lower incidence of GDM. However, increasing physical activity among women on a plant-based diet does not affect the risk of GDM. On the other hand, among women on an omnivore diet, physical activity is associated with a lower incidence of GDM. We did not observe that the type of diet and increased physical activity were additional factors reducing the risk of gestational hypertension. The risk of gestational hypertension is strongly related to BMI, as mentioned above. The study conducted by Kruszewski A, Przybysz P., et al., which included over 960 women, showed that GDM is more common in women who did not exercise at all or had physical activity less than 90 min a week during the 6 months before pregnancy [ 17 ].\n\nThe previous studies on the impact of maternal diet on a newborn’s birth weight were limited and yielded inconsistent findings. Piccoli et al. in a systematic narrative review reported that five studies found lower birth weight in neonates of vegetarian mothers, whereas two analyses suggested higher birth weight [ 14 ]. Our findings showed no association between maternal diet and newborn birth weight. The percentage of newborns with too low body weight (<2500 g) was similar in both subgroups. Moreover, neonates of women on a plant-based diet had similar Apgar score results at the 5th minute after birth compared to neonates of omnivorous women. Newborns who received 8 or more points in the Apgar score constituted 98.8% and 96.6% of the above-mentioned groups, respectively. Moreover, multivariate analysis showed that women with higher prepregnancy BMI on an omnivore diet delivered children in worse condition (Apgar score less than 8 points). We did not observe an association between the type of delivery (vaginal or cesarean section) and maternal diet. In a multivariate analysis, a relationship was found between the newborn birth weight and the type of delivery.\n\nAccording to a paper by Kesary et al., a maternal vegetarian diet was associated with a lower risk of excessive weight gain, and there was no statistical evidence for an association between maternal diet and preterm delivery or low birth weight [ 13 ]. We did not observe an increased risk of preterm birth in the group of women on a plant-based diet compared to omnivorous women in univariate analysis, but multivariate analysis revealed that prepregnancy BMI was a contributory factor influencing the pregnancy duration in diet type subgroups, i.e., overweight and obese women on an omnivore diet more frequently delivered prematurely and post-term. The study by Yisahak et al. also showed that diet-based full vegetarians had marginally increased odds of inadequate gestational weight gain during the second trimester [ 22 ]. Our univariate analysis of the Polish population showed that the type of diet 6 months before conception did not impact weight gain during pregnancy. Multivariate analysis revealed an influence of prepregnancy BMI on the relationship between diet type and gestational weight gain: overweight and obese women on an omnivore diet gained too much weight more frequently, and similarly, overweight women presented insufficient weight gain on an omnivore diet.\n\nThe questionnaire used in this study was self-composed by the authors and it had not been previously validated in a pregnant population. The limitation was that we could not verify all the answers. Some answers were subjective and self-reported by participants. The limitation of our survey was the fact that women could only choose the way of eating in closed questions distinguishing between a meat and a meatless diet, and women did not specify what type of food they consumed. We cannot rule out that a confounding bias and a misclassification bias may have occurred because of this. Unfortunately, we have no information on whether both types of diet were well-balanced and provided all the necessary micronutrients. An additional limitation was no information about the caloric content of the diet.\n\nIn a study by Marangoni F. et al., it was observed that even in the most industrialized countries, specific dietary intakes during pregnancy and lactation are often inadequate. This particularly applies to DHA, calcium, iron, folic acid, iodine, and vitamin D [ 28 ]. This result coincides with research on the Polish population that showed that none of the studied women managed adequate nutrition in terms of all tested macro- and micronutrients [ 29 ]. Particular attention should be paid to women of childbearing age following exclusion diets such as veganism because of the increased risk of inadequate supply of nutrients. Findings in the meta-analysis by Bhutta et al. confirm that supplementation during pregnancy reduces low birth weight in the population at risk [ 30 ]. Conclusions from the paper by Avnon et al. are that a vegan diet does not change the umbilical cord levels of B12, folic acid, ferritin, and hemoglobin. Moreover, at greater risk of B12 deficiency are vegans who do not take any vitamin supplementation compared with omnivores [ 31 ].\n\nThe WHO recommends initiation of breastfeeding within 1 h after birth, exclusive breastfeeding of infants till 6 months of age, and continued breastfeeding until 2 years of age or older [ 32 ]. Our research showed that a maternal plant-based diet before conception and during pregnancy is not associated with the occurrence of breastfeeding difficulties.\n\nOur analysis showed that, despite the abundant evidence stating that a plant-based diet during pregnancy is safe for both the mother and the fetus, many women refrain from continuing this diet after conception. As many as one in seven women (14.5%) on a meat-free diet switched to an omnivore diet after becoming pregnant. It is worth considering why women adjust their dietary habits. Our study showed that only 36.8% of surveyed women received advice about nutrition during pregnancy from a healthcare professional such as a doctor, midwife, or dietician. Lack of adequate dietary counseling could be the reason for preference for extensive dietary changes during pregnancy, i.e., reintroducing meat after being vegan or vegetarian.\n\nOur study stands out in that we examined nine associations (in heterogeneous groups, due to exclusions, Figure 1 , Materials and Methods) between the type of diet that women follow during the preconception period and the incidence of pregnancy-complicating diseases, premature birth, type of delivery, and neonatal parameters such as birth weight and Apgar score results. Furthermore, we also evaluated the association between diet and breastfeeding. Overweight women statistically significantly more often were on omnivore than plant-based diets, and this difference between subgroups could be the same limitation in our study. Another limitation could be the fact that the number of women on a plant-based diet is relatively small compared to the number of women in the omnivore group.\n\nThis study aimed to create a scientific paper that would be a compendium of knowledge for women planning pregnancy about the impact and safety of a properly balanced plant-based diet during pregnancy. Our findings are in line with the statements of the American Dietetic Association that well-planned vegetarian diets are appropriate during all stages of the life cycle including pregnancy [ 33 ]. We expect an increase in the population on a plant-based diet. In the coming years, the number of diet-related diseases will change.\n\n— Source (discussion, peer-reviewed): Paulina Przybysz, Adrian Kruszewski, Joanna Kacperczyk-Bartnik, et al. · (2023) · \"The Impact of Maternal Plant-Based Diet on Obstetric and Neonatal Outcomes—A Cross-Sectional Study\" · Nutrients · doi: 10.3390/nu15224717 · PMCID: PMC10675710 · PMID: 38004112\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13025508-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC13025508", "pmid": "41892279", "doi": "10.3390/cells15060488", "title": "Therapeutic Activities of Multipotent Stromal Cells for Islet Regeneration", "journal": "Cells", "publication_year": 2026, "citation": "Nazihah Rasiwala, Gillian I. Bell, Nouran N. Al-Banaa, et al. · (2026) · \"Therapeutic Activities of Multipotent Stromal Cells for Islet Regeneration\" · Cells · doi: 10.3390/cells15060488 · PMCID: PMC13025508 · PMID: 41892279", "question": "Summarize the abstract of the paper titled \"Therapeutic Activities of Multipotent Stromal Cells for Islet Regeneration\".", "answer": "Diabetes mellitus is a global healthcare issue of epidemic proportions. At the root of these disorders, characterized by poor glucose regulation and insulin deficiencies, is the pancreatic beta cell and insufficient insulin signal transduction in peripheral tissues. Residual c-peptide secretion and persisting beta cells have been found in patients who have been living with type 1 diabetes for over 50 years. Thus, beta cell regeneration has been vastly studied in rodents, and many agents to expand beta cell mass are under rigorous investigation for the treatment of diabetes. Multipotent stromal cells (MSC), isolated from human bone marrow, have an immunomodulatory and pro-regenerative secretome that can aid in repairing damaged tissues, including pancreatic islets. MSC transplantation has been shown to reduce hyperglycemia and orchestrate islet repair in experimental diabetes models and is currently being assessed in clinical trials. While the immunomodulatory mechanisms of MSC are well-studied, the beta-cell-regenerative mechanisms are unknown. MSC likely play a regenerative role by signaling to resident progenitor or precursor cells in the pancreas; however, the decades-long controversy surrounding the origin of regenerated adult beta cells remains unresolved. Herein, we take a deep dive into the role of MSC in the treatment of diabetes and the potential cellular mechanisms behind the MSC stimulation of beta cell regeneration.\n\n— Source (abstract, peer-reviewed): Nazihah Rasiwala, Gillian I. Bell, Nouran N. Al-Banaa, et al. · (2026) · \"Therapeutic Activities of Multipotent Stromal Cells for Islet Regeneration\" · Cells · doi: 10.3390/cells15060488 · PMCID: PMC13025508 · PMID: 41892279\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-11782313-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC11782313", "pmid": "39570544", "doi": "10.1007/s12325-024-03050-1", "title": "Investigation of Severe Hypoglycemia Risk Among Patients with Diabetes Treated with Ultra-Rapid Lispro in Japan", "journal": "Advances in Therapy", "publication_year": 2024, "citation": "Seiko Mizuno, Machiko Minatoya, Satoshi Osaga, et al. · (2024) · \"Investigation of Severe Hypoglycemia Risk Among Patients with Diabetes Treated with Ultra-Rapid Lispro in Japan\" · Advances in Therapy · doi: 10.1007/s12325-024-03050-1 · PMCID: PMC11782313 · PMID: 39570544", "question": "What is the published background on \"Investigation of Severe Hypoglycemia Risk Among Patients with Diabetes Treated with Ultra-Rapid Lispro in Japan\"? Cite a peer-reviewed source.", "answer": "The Japanese Clinical Practice Guidelines for Diabetes 2019 recommend treating type 1 diabetes (T1D) with insulin therapy, and type 2 diabetes (T2D) with oral hypoglycemic agents, insulin therapy, or glucagon-like peptide 1 receptor agonists [ 1 ]. Ultra-rapid lispro (URLi), a novel ultra-rapid insulin lispro formulation launched on June 17, 2020, in Japan [ 2 ], improves post-prandial glucose control by closely matching physiological insulin secretion [ 3 ].\n\nHypoglycemia, i.e., a blood glucose level of < 70 mg/dL, is a major side effect of insulin therapy (including URLi); it is classified into non-severe and severe hypoglycemia based on the level of assistance required [ 1 , 4 ]. Non-severe hypoglycemia can be resolved by self-administering oral carbohydrates; however, severe hypoglycemia requires assistance from others to administer glucagon, glucose, or other medical treatments [ 1 , 4 ]. Since severe hypoglycemia can lead to loss of consciousness, seizures, coma, or death [ 5 , 6 ], it is listed as an important identified risk in URLi’s Japan risk management plan (data on file).\n\nIn clinical trials, the incidence rate of severe hypoglycemia in URLi-treated patients ranged from 2.4 to 17.6 per 100 person-years, and the incidence proportion ranged from 0.9 to 7.3% [ 7 – 13 ], due to differences in diabetes type, study period, and drug administration. Among insulin-treated patients with diabetes, the incidence rate of severe hypoglycemia differs in the real world (0.0–1.6 episodes/patient/year) and in controlled clinical trials (0.0–0.5 episodes/patient/year) [ 14 ]. Hence, it is necessary to evaluate the real-world risk of hypoglycemia by analyzing health records or medical claims, as conducted in the past [ 15 , 16 ].\n\nTo our knowledge, there is no information on the incidence of severe hypoglycemia in patients receiving URLi in the real-world setting. Furthermore, no study to date has compared the risk of severe hypoglycemia after treatment with URLi versus other rapid-acting insulin analogs (RAIAs). Hence, this post-marketing safety study assessed the incidence proportion and incidence rate of the first severe hypoglycemia event requiring a hospital visit for URLi-treated patients (i.e., a descriptive analysis). This study also compared the risk of severe hypoglycemia among patients treated with URLi or other RAIAs (i.e., a comparative analysis). Considering the diverse treatment regimens in the real world, this study also evaluated the aforementioned objectives in multiple subgroups as described later.\n\n— Source (introduction, peer-reviewed): Seiko Mizuno, Machiko Minatoya, Satoshi Osaga, et al. · (2024) · \"Investigation of Severe Hypoglycemia Risk Among Patients with Diabetes Treated with Ultra-Rapid Lispro in Japan\" · Advances in Therapy · doi: 10.1007/s12325-024-03050-1 · PMCID: PMC11782313 · PMID: 39570544\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13116625-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC13116625", "pmid": "42073989", "doi": "10.3390/ijms27083346", "title": "Amino Acid Dysregulation in the Mother–Fetus Unit: Multi-Compartment Metabolomic Signatures of Gestational Diabetes Mellitus and Fetal Macrosomia", "journal": "International Journal of Molecular Sciences", "publication_year": 2026, "citation": "Natalia A. Frankevich, Alisa O. Tokareva, Anna A. Derenko, et al. · (2026) · \"Amino Acid Dysregulation in the Mother–Fetus Unit: Multi-Compartment Metabolomic Signatures of Gestational Diabetes Mellitus and Fetal Macrosomia\" · International Journal of Molecular Sciences · doi: 10.3390/ijms27083346 · PMCID: PMC13116625 · PMID: 42073989", "question": "What did the discussion section of the paper \"Amino Acid Dysregulation in the Mother–Fetus Unit: Multi-Compartment Metabolomic Signatures of Gestational Diabetes Mellitus and Fetal Macrosomia\" cover?", "answer": "The main risk factors for GDM in the studied cohort were high risk of PE (OR ≈ 6.75), family history of diabetes (OR ≈ 3.9), and elevated pre-pregnancy and delivery BMI. The heterogeneity of GDM is supported by the substantial proportion of women with normal weight (54%). Shared pathogenetic mechanisms with PE, evidence of systemic inflammation, and residual metabolic imbalance despite treatment underscore the need for improved therapeutic strategies. The absence of differences in most obstetric outcomes reflects the effectiveness of timely diagnosis and therapy.\n\nThese findings are fully consistent with the contemporary concept of GDM as a heterogeneous condition requiring a personalized approach. The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study [ 23 ] demonstrated that the long-term consequences of GDM for mothers (risk of type 2 diabetes mellitus, cardiovascular disease) and offspring (obesity, impaired glucose tolerance) depend not only on the degree of hyperglycemia but also on baseline metabolic status, gestational weight gain, and genetic factors. The differences observed between subgroups 3 and 4 in the present study confirm the existence of distinct GDM phenotypes: “compensated” (with weight control and dietary therapy) and “decompensated” (with pathological weight gain, elevated glucose levels, and FM). This aligns with recent work in this area [ 24 , 25 ].\n\nCurrent international guidelines (NICE, ACOG, FIGO) emphasize the need for a comprehensive approach to managing pregnant women with GDM, including not only glycemic control but also monitoring of gestational weight gain, screening for urinary tract infections, assessment of coagulation status, and consideration of risk factors such as history of macrosomia and family history of diabetes. The data obtained in this study confirm the importance of each of these components and justify the need for further prospective studies with larger sample sizes to develop more accurate prognostic models and therapeutic strategies.\n\nThis study revealed significant differences in the amino acid profiles of maternal serum, umbilical cord blood, and amniotic fluid between GDM and physiological pregnancies, and established an association between these alterations and the development of FM, opening new perspectives for understanding the pathogenesis of metabolic disturbances and their prediction. The findings demonstrate that GDM is accompanied by profound remodeling of amino acid metabolism, affecting not only the maternal organism but also the fetoplacental unit, with the pattern of these changes differing according to the presence or absence of FM. This allows for consideration of specific amino acids as potential biomarkers for different clinical outcomes. Analysis of maternal serum identified glycine, 1-methylhistidine, γ-aminobutyric acid, lysine, and tryptophan as the most informative GDM markers, with all except tryptophan showing statistically significant concentration decreases during GDM development. This finding aligns with the current understanding of enhanced amino acid consumption by the fetoplacental complex and impaired amino acid synthesis under conditions of insulin resistance [ 26 , 27 ].\n\nOf particular note is the observed differential dynamics of lysine and 1-methylhistidine, which not only decreased in GDM overall but also exhibited specific alterations in the subgroup of women delivering normal-weight newborns, indicating the existence of distinct metabolic phenotypes within the GDM group and underscoring the heterogeneity of this condition. Analysis of the amino acid profile in umbilical cord blood revealed a substantially broader spectrum of alterations, including glutamine, glycine, asparagine, methionine, aspartic acid, γ-aminobutyric acid, glutamic acid, β-alanine, proline, citrulline, and alanine, all of which also showed decreased concentrations in GDM. These processes reflect impaired placental transport and altered metabolism in fetal tissues under conditions of hyperglycemia and hyperinsulinemia [ 28 ]. Of particular interest is the identified association between levels of branched-chain amino acids, specifically leucine and allo-isoleucine, in cord blood and the development of FM, confirming the key role of these compounds in stimulating insulin secretion and activating anabolic processes in the fetal organism, leading to excessive adipose tissue accumulation and increased birth weight [ 14 ].\n\nAnalysis of amniotic fluid identified lysine, threonine, 1-methylhistidine, and histidine as GDM markers; however, a different dynamic was observed here: lysine and 1-methylhistidine levels were significantly increased in GDM, which may be related to enhanced excretion of these amino acids by the fetal kidneys or to alterations in amniotic fluid composition resulting from polyuria characteristic of fetal hyperglycemia [ 29 , 30 ]. Interestingly, the GDM group subsequently delivering macrosomic infants was characterized by low levels of homocitrulline, asparagine, aminobutyric acid, and lysine, alongside high histidine concentrations, whereas the opposite pattern predominated in the GDM group without macrosomia. This suggests distinct metabolic trajectories leading to excessive fetal weight gain and opens opportunities for early risk stratification.\n\nCorrelation analysis revealed a complex network of relationships between clinical parameters and amino acid profiles, with the strongest negative correlations observed between total protein and fibrinogen concentrations in maternal blood and the levels of numerous amino acids in both maternal and umbilical cord serum. This reflects the tight integration of protein and amino acid metabolism and their coordinated regulation under conditions of metabolic stress [ 31 ].\n\nOf particular interest are the observed correlations between newborn birth weight and concentrations of specific amino acids. Interestingly, maternal BMI both before pregnancy and at delivery showed weak but statistically significant correlations with a limited spectrum of amino acids, predominantly 3-aminoisobutyric acid and 2-aminoadipic acid, whereas gestational weight gain was associated with a broader range of metabolites, including proline, tyrosine, phenylalanine, and methionine. This underscores the importance of dynamic changes in body weight, rather than baseline anthropometric measures alone, in shaping the amino acid profile [ 32 ]. Summary Table S4 presents alterations in amino acid levels across the three biological compartments (maternal serum, umbilical cord serum, amniotic fluid) in GDM, as well as features characteristic of GDM cases complicated by FM.\n\nThe metabolic pathway enrichment analysis using the SMPDB identified key biochemical processes disrupted in GDM and in GDM with FM. Markers of GDM in maternal serum were primarily associated with biotin metabolism, glutamate metabolism, and carnitine synthesis, whereas markers in cord blood enriched a broader spectrum of pathways, including amino acid metabolism, purine metabolism, and amino sugar metabolism, reflecting the systemic nature of metabolic disturbances in the fetus. In amniotic fluid, GDM markers were associated with biotin metabolism, phenylacetate metabolism, aspartate metabolism, and the ammonia cycle, whereas in GDM with FM, the methylhistidine metabolism pathway was additionally enriched. This may be directly related to altered muscle metabolism and changes in body composition in macrosomic newborns. Summary data are presented in Table S5 .\n\nThe observed changes in the amino acid profiles within the maternal–fetal dyad provide critical insights into the mechanistic links between maternal metabolic dysregulation and excessive fetal growth [ 33 ]. These findings can be interpreted within the framework of key signaling pathways that integrate nutrient sensing with cellular growth and metabolism. The mammalian target of rapamycin (mTOR) pathway serves as a central nutrient sensor, particularly sensitive to amino acid availability, and plays a critical role in placental function and fetal growth [ 34 ]. Our observation of decreased branched-chain amino acid (BCAA; leucine, isoleucine, valine) levels in umbilical cord blood in gestational diabetes mellitus (GDM), alongside elevated leucine and allo-isoleucine, particularly in cases of macrosomia, is highly relevant to mTOR signaling. Leucine is a potent activator of mTOR complex 1 (mTORC1) through its interaction with sestrin 2, which relieves inhibition of mTORC1 [ 35 ]. In the placenta, mTORC1 activity regulates system A and system L amino acid transporters, establishing a positive feedback loop in which amino acid availability modulates transporter expression, which in turn determines nutrient delivery to the fetus [ 36 , 37 ]. The elevated leucine levels observed in fetal macrosomia may reflect hyperactivation of placental mTORC1, driving increased amino acid transport and subsequent fetal insulin secretion, thereby promoting anabolic growth. The insulin signaling pathway intersects with amino acid metabolism at multiple levels. Maternal hyperinsulinemia in GDM directly suppresses hepatic gluconeogenesis while simultaneously stimulating protein synthesis in maternal tissues, potentially contributing to the observed reduction in maternal amino acid concentrations. Fetal hyperinsulinemia, a hallmark of fetal macrosomia, further promotes amino acid uptake and protein accretion in fetal tissues [ 38 ]. Our correlation analysis, demonstrating positive associations between fetal weight and lysine (R = 0.45), isoleucine (R = 0.46), and leucine (R = 0.34), supports this mechanism. Conversely, the negative correlation with homocitrulline (R = −0.41) suggests that impaired urea cycle function may accompany excessive anabolic activity.\n\nThe amino acid profile undergoes systemic changes across compartments (mother, umbilical cord, AF); however, these changes are not mirror-like. For example, 1-methylhistidine decreases in maternal blood but increases in AF, highlighting the importance of investigating multiple compartments to understand the complete picture. Decreases in glycine and GABA indicate oxidative stress, inflammation, and impaired neuro/metabolic regulation. Reduced levels of glutamine, asparagine, and citrulline in umbilical cord blood reflect fetoplacental unit dysfunction, including impaired nutrient transport, endothelial dysfunction, and possibly intrauterine fetal metabolic stress.\n\nAmniotic fluid serves as a unique “window” into fetal status. Alterations in AF (increased 1-methylhistidine and lysine) may reflect not so much placental transport as fetal renal function, skin and lung condition, and meconium composition [ 33 ]. This makes AF a valuable specimen for assessing the fetal response to maternal hyperglycemia. The observed changes (particularly glycine and glutamine deficiency) point to potential targets for nutritional intervention or biochemical monitoring aimed at reducing fetal risks. However, this requires further investigation.\n\nThus, the compartment-specific changes we observed reflect differential regulation of amino acid metabolism in maternal and fetal tissues. Decreased glycine and glutamine levels in maternal serum indicate enhanced utilization of gluconeogenic substrates and possible disruption of one-carbon metabolism, with glycine serving as a methyl donor in the methionine cycle and potentially influencing fetal epigenetic programming [ 39 , 40 ]. The significant enrichment of glutamate metabolism pathways among maternal markers is consistent with the role of glutamate as a key nitrogen carrier and precursor for glutathione synthesis, pointing to involvement of oxidative stress [ 41 ]. In umbilical cord blood, the widespread decrease in amino acids, including glutamine, asparagine, and methionine, suggests either impaired placental transport or enhanced fetal utilization, with methionine being critically important for methylation reactions and polyamine synthesis required for rapid fetal growth [ 39 , 42 ]. Enrichment of amino sugar metabolism pathways in umbilical cord blood markers may reflect alterations in glycosylation patterns or remodeling of the extracellular matrix in fetal tissues. Analysis of amniotic fluid reveals unique aspects of fetal excretory function: increased lysine and 1-methylhistidine suggests either fetal polyuria with concentration of these amino acids or altered tubular reabsorption. Histidine, which shows differential patterns in macrosomia, is a precursor of histamine and carnosine involved in antioxidant and anti-inflammatory mechanisms, and the specific enrichment of the methylhistidine metabolism pathway in GDM with macrosomia is particularly interesting, as 3-methylhistidine serves as a marker of myofibrillar protein breakdown [ 43 ], and its elevated level may reflect either increased muscle protein turnover in macrosomic fetuses or subclinical myopathy resulting from chronic hyperglycemic exposure. The distinct metabolic signatures in GDM with and without macrosomia support the concept of GDM heterogeneity: women who develop macrosomia, despite similar glycemic control, exhibit differences in amino acid metabolism that may reflect genetic variations in transporter efficiency or insulin sensitivity. Elevated branched-chain amino acid levels in umbilical cord blood in macrosomia may directly contribute to β-cell hyperplasia and hyperinsulinemia, as leucine allosterically activates glutamate dehydrogenase, potentiating glucose-stimulated insulin secretion, thereby establishing a direct link between maternal amino acid dysregulation and development of the fetal endocrine pancreas [ 44 ]. The inverse correlation of homocitrulline with fetal weight across all compartments warrants particular attention. Homocitrulline is formed by carbamylation of lysine under conditions of oxidative stress, and its low level may indicate either less oxidative protein modification or alterations in urea cycle function [ 45 ]. Amniotic fluid analysis, given its clinical accessibility, has the potential to provide prognostic information regarding the risk of excessive fetal growth. The involvement of specific metabolic pathways such as biotin metabolism, carnitine synthesis, and methylhistidine metabolism may point to potential therapeutic targets in the future, enabling a transition from mere biomarker identification to mechanistic understanding that can serve as a foundation for developing interventional strategies.\n\nAn important methodological limitation for interpretation: all conclusions drawn from this study are preliminary (hypothesis-generating) in nature due to the small sample size. They indicate interesting trends and biological mechanisms that should be confirmed in an independent, larger-scale cohort. It is important to note that in 2025, we published an article entitled “Amino Acid Profile Alterations in the Mother-Fetus System in Gestational Diabetes Mellitus and Macrosomia” [ 15 ], based on the results of a two-center study (Moscow + Tomsk) conducted from January 2024 to March 2025, which included 94 mother–fetus dyads (GDM group: 53, control group: 41; GDM + FM: 23, GDM + normosomia: 30, control: 36). Comparative analysis of data from the Tomsk patient cohort and the Moscow cohort (the present publication) revealed high consensus on key markers: glutamine, histidine, and asparagine were consistently decreased in GDM in maternal blood; isoleucine, leucine, and serine were consistently increased in FM in cord blood and AF; GABA decrease was confirmed in both studies (marker of metabolic dysregulation). Both studies confirm the involvement of amino acid transport, glutamate metabolism, and the urea cycle. Lysine and isoleucine were the most consistent positive correlates of fetal weight; homocitrulline was a consistent negative correlate of fetal weight. Both studies demonstrate high consistency of results, despite different cohorts and sample sizes. The identified markers (glutamine, histidine, asparagine in maternal blood; isoleucine, leucine, serine in cord blood and AF) can be considered valid candidates for the development of diagnostic panels. The differential dynamics of amino acids across different biological compartments underscore the need for a comprehensive approach to assessing the mother–fetus system and open prospects for early diagnosis and personalized correction of metabolic disturbances in GDM and FM.\n\n— Source (discussion, peer-reviewed): Natalia A. Frankevich, Alisa O. Tokareva, Anna A. Derenko, et al. · (2026) · \"Amino Acid Dysregulation in the Mother–Fetus Unit: Multi-Compartment Metabolomic Signatures of Gestational Diabetes Mellitus and Fetal Macrosomia\" · International Journal of Molecular Sciences · doi: 10.3390/ijms27083346 · PMCID: PMC13116625 · PMID: 42073989\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-9883741-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC9883741", "pmid": "36637888", "doi": "10.2196/41235", "title": "Behavior Change Effectiveness Using Nutrition Apps in People With Chronic Diseases: Scoping Review", "journal": "JMIR mHealth and uHealth", "publication_year": 2023, "citation": "Emily Salas-Groves, Shannon Galyean, Michelle Alcorn, et al. · (2023) · \"Behavior Change Effectiveness Using Nutrition Apps in People With Chronic Diseases: Scoping Review\" · JMIR mHealth and uHealth · doi: 10.2196/41235 · PMCID: PMC9883741 · PMID: 36637888", "question": "What is the published background on \"Behavior Change Effectiveness Using Nutrition Apps in People With Chronic Diseases: Scoping Review\"? Cite a peer-reviewed source.", "answer": "Cardiovascular disease (CVD), cancer, diabetes mellitus (DM), and obesity are common chronic diseases [ 1 ], and their prevalence is reaching a substantial epidemic level internationally [ 2 ]. Chronic diseases are defined by the Centers for Disease Control and Prevention broadly as “conditions that last one year or more and require ongoing medical attention or limit activities of daily living or both” [ 3 ]. Chronic diseases affect hospitalization, mortality rates, and people’s overall health and quality of life (QOL) [ 1 ]. For example, CVD remains the most prevalent cause of morbidity and mortality in high-income countries despite significant advances in treatment over the last 5 decades. Recent epidemiological data show that CVD mortality is no longer declining and is indeed rising in some communities [ 4 ], and hospitalization rates are universally increasing [ 5 ]. Furthermore, chronic conditions such as cancer, CVD, DM, and chronic respiratory diseases caused approximately 33.2 million deaths worldwide in 2019 [ 6 ]. The prevalence of obesity has increased in all World Health Organization regions since 2000, which affects other chronic conditions as it is a risk factor for the development of CVD, DM, and several cancers [ 6 ].\n\nAs the impact of chronic diseases continues to increase, finding strategies to improve care, access to care, and patient empowerment becomes increasingly essential. Therefore, mobile health (mHealth) technology is rapidly gaining popularity among health care providers and consumers [ 7 ]. mHealth technology is defined as mobile devices (ie, mobile phones or monitoring devices) intended to be worn, carried, or accessed by patients or health care providers to monitor health status or improve health outcomes [ 8 ]. Among mobile devices, the most used are smartphones, with more than three-quarters of Americans having one, and at least one-third of smartphone owners use a health app [ 7 , 9 ]. Health care providers use mHealth to access clinical information, collaborate with care teams, communicate over long distances with patients, and facilitate real-time monitoring and interventions. These apps provide an opportunity to increase health care access for vulnerable populations [ 10 ]. Patients use mHealth to track their health data, access their clinical records, and communicate with their providers [ 11 ].\n\nFurthermore, a meta-analysis [ 12 ] reported promising results for mHealth interventions in the improvement of patient outcomes such as body measurements (ie, weight and waist circumference), metabolic and physiological measurements (ie, blood pressure and glucose levels), adherence to and safe use of medication, physical activity performance, meal management, and awareness of health conditions and treatment options. Mobile apps that provide tools intended to facilitate nutrition care via smartphone technologies provide patients with more autonomy, thus empowering them and offsetting patient disengagement [ 13 ]. Moreover, mobile app–based interventions effectively improve diet and diet-related health outcomes, and effect sizes are comparable with those of traditional nondigital interventions [ 14 ]. For example, mHealth interventions can help improve lifestyle behaviors related to CVD [ 15 , 16 ]. A recent meta-analysis [ 17 ] found that using mHealth interventions for CVD was associated with improved blood pressure and hospitalization rates. In addition, mHealth apps have emerged as supportive tools in managing cancer as they reduce the financial burden, provide access to information, and facilitate communication [ 18 ]. Different studies and meta-analyses of patients with cancer have shown the benefits of mHealth, which include reducing fatigue or pain [ 19 , 20 ], providing distance physical activity programs [ 21 , 22 ], the use of social networks to improve QOL [ 23 ], and monitoring of symptoms [ 24 ]. mHealth offers improved and cost-effective care to people with type 2 DM (T2DM) through improved diabetes self-management [ 25 , 26 ]. These apps seem to increase the perception of self-care by contributing to better knowledge among people with T2DM [ 10 ]. Individuals with DM also become more confident in dealing with their illness, primarily because of decreased fear resulting from a lack of information [ 27 , 28 ]. For obesity, a systematic review [ 29 ] has found that technology-based interventions can provide a moderately effective way of facilitating lifestyle changes and weight loss. New technologies could help reduce economic costs, improve accessibility and adherence to treatment, and increase patient motivation and weight control [ 30 ].\n\nThe use of mobile apps for mHealth and of general health apps is increasing rapidly. However, these apps focus on improving general health care concerns, with limited apps focusing on specific chronic diseases and their nutritional intervention. The available evidence on the effectiveness of mHealth apps toward behavior change to improve chronic disease outcomes is also limited. Systematic reviews to date regarding nutrition apps have focused on healthy participants or examined the effects of dietary apps on diet improvement but not on chronic diseases [ 31 ]. Most reviews were inconclusive, with the authors recommending further research in this area to demonstrate possible benefits [ 32 - 34 ]. From a clinical point of view, it is essential to know if an app designed for chronic diseases produces behavior changes to improve an individual’s chronic disease outcomes. From an app creator’s point of view, it is crucial to see what needs to be done when developing an app directed toward people with chronic diseases to enhance the app’s effectiveness on behavior change and produce positive outcomes. The goal of this review was to define behavioral theories associated with mHealth use, evaluate behavior change techniques (BCTs), and describe the behavior change effectiveness using mHealth nutrition interventions in people with chronic diseases (ie, CVD, DM, cancer, and obesity).\n\n— Source (introduction, peer-reviewed): Emily Salas-Groves, Shannon Galyean, Michelle Alcorn, et al. · (2023) · \"Behavior Change Effectiveness Using Nutrition Apps in People With Chronic Diseases: Scoping Review\" · JMIR mHealth and uHealth · doi: 10.2196/41235 · PMCID: PMC9883741 · PMID: 36637888\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12901260-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12901260", "pmid": "40418292", "doi": "10.1007/s00246-025-03882-w", "title": "Association Between Sphericity and Ventricular Function in Fetus of Diabetic Mother: A Longitudinal Study from Fetal to Neonatal Period", "journal": "Pediatric Cardiology", "publication_year": 2025, "citation": "Ayman F. Sabry, Patrick D. Evers, Erin J. Madriago · (2025) · \"Association Between Sphericity and Ventricular Function in Fetus of Diabetic Mother: A Longitudinal Study from Fetal to Neonatal Period\" · Pediatric Cardiology · doi: 10.1007/s00246-025-03882-w · PMCID: PMC12901260 · PMID: 40418292", "question": "What is the published background on \"Association Between Sphericity and Ventricular Function in Fetus of Diabetic Mother: A Longitudinal Study from Fetal to Neonatal Period\"? Cite a peer-reviewed source.", "answer": "Diabetes mellitus (DM) is a relatively common medical disorder of pregnancy affecting about 7% of the pregnant population and it includes pregestational diabetes (PGD) and gestational diabetes mellitus (GDM) [ 1 , 2 ]. DM not only leads to maternal complications in later life of mother but also immediate and later fetal complications [ 2 , 3 ]. In all the diabetic pregnancies GDM accounts for more than 80% and the rest are PGD (type I and type II) [ 1 ]. In PGD, high maternal glucose level appears before pregnancy; in contrast to GDM, abnormal maternal glucose level starts from second to third trimester [ 2 , 3 ].\n\nDM is a systemic chronic metabolic disorder characterized by increased insulin resistance and/or β-cell defects [ 4 , 5 ]. Intrauterine exposure to high level of maternal blood glucose significantly increases the insulin secretion in fetal pancreas, leading to fetal hyperinsulinemia, and the fetal heart is one of the major organs affected by hyperinsulinemia [ 3 – 5 ]. The rapid cell proliferation and differentiation during fetal growth are very sensitive to any changes in environment leading to permanent alteration in the cardiac structural and functional constitution [ 5 – 7 ].\n\nCardiac function impairment in the fetus of the diabetic mother during the second and third trimester is well established and the timing and severity of hyperglycemia in relation to gestational age are a critical factor that determines these effects [ 8 , 9 ]. The diastolic dysfunction represents the earliest manifestation of diabetic cardiomyopathy, preceding the systolic dysfunction [ 9 , 10 ]. Ventricular remodeling encompasses alternation in ventricular mass, shape, and geometry as a result of an increased hemodynamic load, neurohormonal activation, and genetic factors [ 11 – 13 ]. The sphericity index (SI) is used to evaluate the change of the shape of the right and left ventricles [ 11 , 12 ]. Less is known about changes in ventricular geometry and remodeling during fetal life among different diabetic levels and its association with cardiac dysfunction and the persistence of these changes in neonatal period.\n\nTherefore, the purpose of this study was to provide a detailed overview of the fundamental mechanism of ventricular remodeling and its relation to cardiac function for different types and levels of DM during pregnancy and postnatally.\n\n— Source (introduction, peer-reviewed): Ayman F. Sabry, Patrick D. Evers, Erin J. Madriago · (2025) · \"Association Between Sphericity and Ventricular Function in Fetus of Diabetic Mother: A Longitudinal Study from Fetal to Neonatal Period\" · Pediatric Cardiology · doi: 10.1007/s00246-025-03882-w · PMCID: PMC12901260 · PMID: 40418292\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12400561-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC12400561", "pmid": "40887640", "doi": "10.1186/s12887-025-06018-4", "title": "Impact of tailored diabetes education on adherence and glycemic control in children and adolescents on continuous subcutaneous insulin infusion, prospective interventional study in a tertiary center", "journal": "BMC Pediatrics", "publication_year": 2025, "citation": "Mona Hassan, Mahmoud ElHelaly, Nora Badawi, et al. · (2025) · \"Impact of tailored diabetes education on adherence and glycemic control in children and adolescents on continuous subcutaneous insulin infusion, prospective interventional study in a tertiary center\" · BMC Pediatrics · doi: 10.1186/s12887-025-06018-4 · PMCID: PMC12400561 · PMID: 40887640", "question": "Summarize the abstract of the paper titled \"Impact of tailored diabetes education on adherence and glycemic control in children and adolescents on continuous subcutaneous insulin infusion, prospective interventional study in a tertiary center\".", "answer": "Structured diabetes education plays a crucial role in the management of Type 1 Diabetes (T1D), especially with advanced technologies such as continuous subcutaneous insulin infusion (CSII). This study evaluates the impact of tailored education on adherence and glycemic control among pediatric CSII users.\n\nThis interventional analytical study included 30 patients diagnosed with T1D with age ranged from 5 to 18 years, recruited from Diabetes & Endocrinology Clinic at tertiary university-based children’s hospital. Patients were recruited for one year duration. Patients who were on multiple daily injection (MDI) for 2 to 10 years were shifted to CSII after receiving comprehensive diabetes education. Their education level was assessed individually using a questionnaire to assess patients’ knowledge and application skills at the time of insulin pump insertion, 3 and 6 months later. Twenty-five patients were on mini-med 715, 10 patients used flash glucose monitoring, and 15 patients used self-monitoring blood sugar, while five patients were on mini-med 780G and continuous glucose monitoring (CGM) using guardian 4 (G4).\n\nStudy included 19 females (63.3%) and 11 males (36.7%) with age ranged from 7 to 11 with mean ± SD of 10.74 ± 1.86. Patients’ education level was assessed before pump insertion, and 3 months later which shows significant improvement in patients’ diabetes knowledge and technical skills with P-value 0.038. Also, time in range (TIR) improved significantly in well-educated patients at 3 and 6 months with P-values 0.048 and 0.025 respectively. There was highly significant improvement of HbA1c after 6 months (8.82 ± 1.5 vs. 7.18 ± 0.56) with P-value 0.000 after receiving diabetes education.\n\nTailored diabetes education significantly improves adherence and glycemic outcomes in pediatric patients using CSII. Integrating structured educational programs with diabetes technology is essential to achieve optimal metabolic control in youth.\n\n— Source (abstract, peer-reviewed): Mona Hassan, Mahmoud ElHelaly, Nora Badawi, et al. · (2025) · \"Impact of tailored diabetes education on adherence and glycemic control in children and adolescents on continuous subcutaneous insulin infusion, prospective interventional study in a tertiary center\" · BMC Pediatrics · doi: 10.1186/s12887-025-06018-4 · PMCID: PMC12400561 · PMID: 40887640\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12572562-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC12572562", "pmid": "39849203", "doi": "10.1007/s10278-025-01386-w", "title": "Wound Segmentation with U-Net Using a Dual Attention Mechanism and Transfer Learning", "journal": "Journal of Imaging Informatics in Medicine", "publication_year": 2025, "citation": "Rania Niri, Sofia Zahia, Alessio Stefanelli, et al. · (2025) · \"Wound Segmentation with U-Net Using a Dual Attention Mechanism and Transfer Learning\" · Journal of Imaging Informatics in Medicine · doi: 10.1007/s10278-025-01386-w · PMCID: PMC12572562 · PMID: 39849203", "question": "Summarize the abstract of the paper titled \"Wound Segmentation with U-Net Using a Dual Attention Mechanism and Transfer Learning\".", "answer": "Accurate wound segmentation is crucial for the precise diagnosis and treatment of various skin conditions through image analysis. In this paper, we introduce a novel dual attention U-Net model designed for precise wound segmentation. Our proposed architecture integrates two widely used deep learning models, VGG16 and U-Net, incorporating dual attention mechanisms to focus on relevant regions within the wound area. Initially trained on diabetic foot ulcer images, we fine-tuned the model to acute and chronic wound images and conducted a comprehensive comparison with other state-of-the-art models. The results highlight the superior performance of our proposed dual attention model, achieving a Dice coefficient and IoU of 94.1% and 89.3%, respectively, on the test set. This underscores the robustness of our method and its capacity to generalize effectively to new data.\n\n— Source (abstract, peer-reviewed): Rania Niri, Sofia Zahia, Alessio Stefanelli, et al. · (2025) · \"Wound Segmentation with U-Net Using a Dual Attention Mechanism and Transfer Learning\" · Journal of Imaging Informatics in Medicine · doi: 10.1007/s10278-025-01386-w · PMCID: PMC12572562 · PMID: 39849203\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12812715-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC12812715", "pmid": "41561040", "doi": "10.3389/fendo.2025.1691740", "title": "Effects of Lenvatinib treatment for advanced differentiated thyroid cancer on cortisol deficiency", "journal": "Frontiers in Endocrinology", "publication_year": 2026, "citation": "Salvatore Monti, Beatrice Fazzalari, Valerio Renzelli, et al. · (2026) · \"Effects of Lenvatinib treatment for advanced differentiated thyroid cancer on cortisol deficiency\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2025.1691740 · PMCID: PMC12812715 · PMID: 41561040", "question": "What did the discussion section of the paper \"Effects of Lenvatinib treatment for advanced differentiated thyroid cancer on cortisol deficiency\" cover?", "answer": "Among the adverse events evaluated during Lenvatinib treatment, routine monitoring of adrenal function is not commonly performed in real life; however, recent evidence from relatively small series of patients with advanced thyroid cancer has suggested a potential impact of Lenvatinib on development of PAI and fatigue ( 5 – 9 ).\n\nIt is now recognized that PAI can occur with Lenvatinib treatment, but its clinical significance remains unclear. Consequently, PAI is not always investigated in patients receiving Lenvatinib, which may delay diagnosis.\n\nPAI is a serious and potentially life-threatening condition, and its simultaneous occurrence in patients with RR-DTC could have a profoundly negative impact on the morbidity and mortality of those treated with Lenvatinib, by increasing drug-related toxicity. In this context, early diagnosis plays a crucial role.\n\nIn this prospective study, using the current Endocrine Society Clinical Practice Guideline ( 12 ), we observed a higher prevalence (77.4%) of PAI-18.1 in patients with peak cortisol levels below 500 nmol/L (18.1 mcg/dL) compared to previous reports. This is likely because we routinely monitor adrenal function with ACTH stimulation testing more frequently than other studies, which often assess adrenal function only when ACTH levels are elevated.\n\nOur study design therefore allows early identification of mild PAI cases. Furthermore, repeated ACTH stimulation tests performed during follow-up consistently confirmed the diagnosis of PAI and demonstrated a progressive decline in cortisol response during Lenvatinib treatment.\n\nThe mechanisms underlying Lenvatinib-induced PAI remain unknown. Lenvatinib is a multitargeted tyrosine kinase inhibitor (TKI); notably, two of its targets—the vascular endothelial growth factor receptors (VEGFRs) and platelet-derived growth factor receptor alpha (PDGFRα)—may be involved in adrenal regulation ( 14 , 15 ). A key role seems to be played by the reduction of vascular density, mainly due to VEGF inhibition, causing ischemic damage to the adrenal cortex. Interestingly, a study in mice showed recovery of vascular damage following Lenvatinib withdrawal ( 16 ).\n\nThis experimental study supports the possibility that the adverse effect of Lenvatinib on adrenal function may be transient and dose-dependent, with recovery of adrenal function following drug discontinuation, as is common with other treatment-related adverse events. Notably, in one of our patients with PAI, Lenvatinib was interrupted for 34 days after one year of treatment due to surgical complications following laparoscopic cholecystectomy. After appropriate discontinuation of cortisone acetate, repeated ACTH stimulation test showed normal peak cortisol levels (597.9 nmol/L). Lenvatinib was then resumed at the previous dose (14 mg). However, after three months of reinitiation, two consecutive ACTH stimulation tests revealed a recurrence of PAI.\n\nThe strength of our study is the ability to evaluate adrenal function both before and during treatment with Lenvatinib. All our patients had normal adrenal function prior to starting Lenvatinib. Moreover, none of the patients presented with adrenal metastases or other adrenal gland abnormalities that could cause PAI, as confirmed by whole-body CT scans and whole-body 18F-FDG PET/CT during follow-up. Together, these findings support the conclusion that PAI is induced by Lenvatinib.\n\nIn recent years, there has been a proposal to lower the serum cortisol cut-off for the diagnosis of primary adrenal insufficiency (PAI) compared to the threshold established in the 2016 Endocrine Society Clinical Practice Guideline ( 12 ). While using an ACTH-stimulated peak cortisol threshold of 18 mcg/dL (500 nmol/L) to exclude adrenal insufficiency minimizes missed diagnoses, it may lead to overdiagnosis when more specific assays are employed. Consequently, several recent studies utilizing more specific (less cross-reactive) cortisol assays have suggested lowering the ACTH-stimulated peak cortisol cut-off to between 14 mcg/dL (386.2 nmol/L) and 15 mcg/dL (413.8 nmol/L) to reduce false-positive results in ACTH stimulation tests ( 13 , 17 ).\n\nIn this context, we applied an ACTH-stimulated peak cortisol cut-off of 14 mcg/dL as a diagnostic criterion for PAI (PAI-14). As expected, the prevalence of PAI-14 was lower than that of PAI-18.1; however, it remained substantial, with 14 out of 31 patients (45.2%) meeting the PAI-14 criterion.\n\nThe diagnosis of PAI-14 was preceded, on average, by an increase in ACTH levels 11.77 ± 8.38 months earlier in 92.3% of cases. This rise was greater, although not statistically significant (p = 0.054), compared to the increase observed before the diagnosis of PAI-18.1, which occurred in only 62.5% of cases and on average 6.28 ± 5.69 months earlier.\n\nThis observation indicates that cortisol deficiency is, as expected, more pronounced in PAI-14 than in PAI-18.1. Indeed, cortisol deficiency leads to reduced negative feedback on the hypothalamic-pituitary axis and a consequent compensatory increase in ACTH levels, reflecting greater biochemical and clinical impairment of PAI ( 12 ).\n\nTreatment with cortisone acetate (CA) resulted in a significant improvement in fatigue, particularly during the first 3 months of therapy, with benefits persisting in the majority of cases, especially among patients with PAI-14.\n\nFatigue is one of the most common treatment-related adverse events, with a reported prevalence of up to 90–100% of cases ( 18 – 22 ). The wide variability in fatigue prevalence reported in the literature is partly due to the frequent underestimation and underdiagnosis of fatigue in clinical practice, despite it being a distressing and disabling condition.\n\nFatigue is a major cause of dose reduction, interruption, or discontinuation of Lenvatinib treatment, potentially leading to decreased treatment efficacy and shorter progression-free survival (PFS) ( 4 ). Managing fatigue effectively is critical to maintain optimal treatment adherence and maximize clinical benefit ( 23 ).\n\nThe mechanisms underlying fatigue are not yet fully elucidated. Fatigue arises from a complex interplay of multiple factors, including physical, psychological and biochemical conditions ( 24 ).\n\nThis study confirms that in the presence of fatigue, it is necessary to exclude PAI. If PAI is diagnosed, prompt initiation of glucocorticoid replacement therapy is essential to manage fatigue in Lenvatinib treatment.\n\nBased on current evidence, we propose that all patients considered for Lenvatinib treatment undergo evaluation of adrenal function using a 250 μg ACTH stimulation test along with serum ACTH level measurement. A cortisol peak greater than 646.6 nmol/L indicates a low risk (approximately 30%) of developing PAI. In such cases, if ACTH levels are within the normal range, repeat ACTH stimulation testing is not mandatory; however, if ACTH levels are elevated beyond the upper limit of normal, ACTH stimulation testing should be repeated within 3 to 6 months.\n\nConversely, a cortisol peak below 646.6 nmol/L suggests a high risk (about 70%) of PAI development. For these patients, ACTH stimulation tests should be repeated according to ACTH concentrations: if ACTH is normal, retesting may be delayed but should occur within 6 to 12 months; if ACTH levels are elevated, repeat ACTH stimulation should be performed as soon as possible to guide timely diagnosis and management.\n\nThere are some limitations of our study that should be considered. It is a prospective single-center investigation conducted at a tertiary referral center, involving a relatively small sample size of 31 patients, which may limit the generalizability of the findings to broader populations of patients with RR-DTC treated with Lenvatinib. Additionally, the limited sample size may lack sufficient statistical power to detect weaker associations between PAI development, baseline clinical characteristics, and treatment parameters (e.g., initial dose, dose intensity, duration).\n\nIn conclusion, based on our experience and supported by the literature, we recommend that adrenal function assessment be incorporated into the evaluation of patients treated with Lenvatinib, especially those experiencing fatigue. When PAI is confirmed, initiating glucocorticoid replacement therapy is advisable to manage fatigue and prevent unnecessary dose reduction or discontinuation of Lenvatinib treatment. This approach aligns with findings that PAI is a common and treatable cause of fatigue in this patient population, and that early intervention improves clinical outcomes and quality of life.\n\n— Source (discussion, peer-reviewed): Salvatore Monti, Beatrice Fazzalari, Valerio Renzelli, et al. · (2026) · \"Effects of Lenvatinib treatment for advanced differentiated thyroid cancer on cortisol deficiency\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2025.1691740 · PMCID: PMC12812715 · PMID: 41561040\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12306309-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12306309", "pmid": "40701606", "doi": "10.1136/bmjopen-2024-095100", "title": "eHealth versus face-to-face support for remission of type 2 diabetes by calorie restriction (eHealth DIabetes remission Trial): study protocol for a non-inferiority parallel group randomised controlled trial", "journal": "BMJ Open", "publication_year": 2025, "citation": "Julia Otten, Anna Tellström, Claudia Schien, et al. · (2025) · \"eHealth versus face-to-face support for remission of type 2 diabetes by calorie restriction (eHealth DIabetes remission Trial): study protocol for a non-inferiority parallel group randomised controlled trial\" · BMJ Open · doi: 10.1136/bmjopen-2024-095100 · PMCID: PMC12306309 · PMID: 40701606", "question": "What is the published background on \"eHealth versus face-to-face support for remission of type 2 diabetes by calorie restriction (eHealth DIabetes remission Trial): study…\"? Cite a peer-reviewed source.", "answer": "A breakthrough in the treatment of type 2 diabetes is the recent Diabetes REmission Clinical Trial (DiRECT), which shows that long-term remission of type 2 diabetes can be achieved through calorie restriction. 1 2 The study found that of the people with type 2 diabetes who received total diet replacement with 850 kcal/day over a period of 3 to 5 months, 46% were in diabetes remission after 1 year, and 36% were still in remission after 2 years. 2 Diabetes remission is defined as haemoglobin A1c (HbA1c) below 48 mmol/mol (6.5%) without diabetes medication. 3 The HbA1c value reflects the average plasma glucose level of the last 2 months. In the DiRECT study, the diabetes remission rate was up to 70% in those who had maintained a weight loss of at least 15 kg. 2 Remarkably, the main motivator for study participants to lose weight was to achieve diabetes remission and thus avoid diabetes medication, 4 that is, remission was a much greater source of motivation than the promise that weight loss would reduce the risk of future complications and increase life expectancy.\n\nAccording to a health economic evaluation of the DiRECT study, diabetes remission with total diet replacement is cost-saving after 5–6 years despite face-to-face meetings between patient and healthcare provider every 2 to 4 weeks. 5 Based on the results of the DiRECT study, calorie restriction with the goal of 15 kg weight loss and diabetes remission is now strongly recommended in the treatment guidelines of the European and American Diabetes Associations. 6\n\nAs far as we know, no dietary intervention with the overarching aim of remission of type 2 diabetes has yet been conducted comparing eHealth with face-to-face care. eHealth can have many benefits: It may be more effective than face-to-face care because it eliminates travel time for the patient, and it allows for a more flexible schedule for both the patient and the healthcare provider. In studies where eHealth was used to lower blood glucose levels in people with diabetes, eHealth was superior to conventional care. 7 In addition, a meta-analysis found that prevention of type 2 diabetes through eHealth via weight loss was successful in 63% of interventions in the short term and in 21% in the long term, that is, 12 months or longer. 8 However, only half of the studies were randomised controlled trials, and the control group usually received no intervention. The question of whether an intervention with eHealth support is more effective than face-to-face support is therefore still open.\n\nAfter 3 months of total diet replacement and reaching the weight goal, food is gradually reintroduced for 6 weeks to reduce the risk of regaining weight. One meal at a time is reintroduced over about 2 weeks. During this time, participants receive guidance on how to prepare nutritious, low-calorie meals and snacks that meet the dietary recommendations. To allow flexibility for participants, the food reintroduction phase can be longer or shorter than 6 weeks.\n\n— Source (introduction, peer-reviewed): Julia Otten, Anna Tellström, Claudia Schien, et al. · (2025) · \"eHealth versus face-to-face support for remission of type 2 diabetes by calorie restriction (eHealth DIabetes remission Trial): study protocol for a non-inferiority parallel group randomised controlled trial\" · BMJ Open · doi: 10.1136/bmjopen-2024-095100 · PMCID: PMC12306309 · PMID: 40701606\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13138595-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC13138595", "pmid": "41439610", "doi": "10.1530/ETJ-25-0206", "title": "Low FT4 levels in early pregnancy are associated with higher insulin therapy need in women with gestational diabetes mellitus", "journal": "European Thyroid Journal", "publication_year": 2026, "citation": "Emna Jelloul, Manon Lomré, Pierre Kleynen, et al. · (2026) · \"Low FT4 levels in early pregnancy are associated with higher insulin therapy need in women with gestational diabetes mellitus\" · European Thyroid Journal · doi: 10.1530/ETJ-25-0206 · PMCID: PMC13138595 · PMID: 41439610", "question": "What is the published background on \"Low FT4 levels in early pregnancy are associated with higher insulin therapy need in women with gestational diabetes mellitus\"? Cite a peer-reviewed source.", "answer": "Gestational diabetes mellitus (GDM) is a prevalent complication during pregnancy (11% in Europe doi: 10.3389/fendo.2021.691033.) and known to be associated with higher rates of preeclampsia, macrosomia, and other complications ( 1 ). Similarly, thyroid disorders during pregnancy, including (subclinical) hypothyroidism (SCH) and thyroid autoimmunity (TAI), are common and linked to various adverse pregnancy outcomes, of which some are the same as documented in case of GDM ( 2 ).\n\nThyroid disorders have been associated with a higher risk of GDM via different pathways, due to increased insulin resistance (IR) in case of thyroid dysfunction, and via common inflammatory pathways in case of the presence of TAI ( 3 , 4 ).\n\nThe initial treatment of GDM consists in dietary (Di) and lifestyle (LS) measures (DiLS), and when glycaemic targets as proposed by the international societies are not rapidly reached, insulin therapy (IT) is started ( 5 ).\n\nSeveral factors have been associated with the need for IT in GDM, including advanced maternal age, body mass index (BMI) (obesity) and a history of GDM or familial diabetes ( 6 ).\n\nData on the impact of thyroid dysfunction on the IT need in women with GDM are limited to three studies ( 7 , 8 , 9 ). One in association with women who had hypothyroidism ( 7 ) and two others in case of hypothyroxinaemia ( 8 , 9 ).\n\nWe had two main aims in this study. The first was to compare all baseline data (demographic, obstetric and thyroid) and thyroid disorders between women with GDM in the DiLS group versus the IT group, and the second to determine in logistic regression analyses which independent variables (demographic, obstetric and thyroid parameters/disorders and treatment) were associated with IT need in women with GDM as dependent outcome.\n\n— Source (introduction, peer-reviewed): Emna Jelloul, Manon Lomré, Pierre Kleynen, et al. · (2026) · \"Low FT4 levels in early pregnancy are associated with higher insulin therapy need in women with gestational diabetes mellitus\" · European Thyroid Journal · doi: 10.1530/ETJ-25-0206 · PMCID: PMC13138595 · PMID: 41439610\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12710098-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC12710098", "pmid": "40536048", "doi": "10.1002/ame2.70032", "title": "Establishment of a novel alloxan‐induced rabbit model exhibiting unique diabetic retinal neuropathy features assessed via ERG + VEP", "journal": "Animal Models and Experimental Medicine", "publication_year": 2025, "citation": "Xinlu Li, Xiaojing Dong, Defei Feng, et al. · (2025) · \"Establishment of a novel alloxan‐induced rabbit model exhibiting unique diabetic retinal neuropathy features assessed via ERG + VEP\" · Animal Models and Experimental Medicine · doi: 10.1002/ame2.70032 · PMCID: PMC12710098 · PMID: 40536048", "question": "What did the discussion section of the paper \"Establishment of a novel alloxan‐induced rabbit model exhibiting unique diabetic retinal neuropathy features assessed via ERG + VEP\" cover?", "answer": "DRN, the primary manifestation of ocular diabetic damage, is characterized by dysfunction of retinal neurons and glial cells. 16 , 17 Hyperglycemia initiates a cascade of biochemical events that lead to early neuronal apoptosis and glial activation. 34 These neuroretinal changes emerge before the onset of clinical DR in individuals with diabetes and precede DR microvascular pathology in diabetic mouse models. 57 However, a significant limitation of diabetic rabbit models remains the high mortality rate among experimental animals. 16 , 17\n\nThis study identified that a single 80 mg/kg injection of alloxan resulted in a low mortality rate and a high modeling success rate, indicating its suitability as an optimal dose for establishing diabetic rabbit models. Currently, no reports provide a standardized optimal dosage of alloxan for diabetes induction in rabbits. A notable increase in HbA1c levels was observed in diabetic rabbits following a single intravenous alloxan injection (80 mg/kg). Insulin deficiency caused by pancreatic beta‐cell destruction remains a defining feature of diabetes. HbA1c serves as a critical diagnostic indicator for diabetes and is regarded as more reliable than glucose levels, as it remains elevated despite fluctuations in BGLs in patients with diabetes. Consistent with these findings, Bem et al. 58 reported a similar increase in HbA1c levels in alloxan‐induced diabetic rabbits over 10 weeks. The developed model exhibited sustained hyperglycemia accompanied by a modest elevation in triglyceride levels. Dyslipidemia appeared at an early stage and was aligned with the pattern of diabetic dyslipidemia observed at week 6. Helfenstein et al. 16 demonstrated that rabbits with diet‐induced impaired glucose tolerance developed hypercholesterolemia by week 24. In contrast, the diabetic rabbit model was developed through a high‐sugar, high‐fat diet, resulting in a distinct pathophysiological profile. Hyperglycemia, lipid metabolism disorders, and abnormalities in the insulin signaling pathway are widely recognized as the initiating factors underlying various pathophysiological changes in DRN (Figure 3A–D ). Notably, progressive retinal changes in DRN are closely associated with elevated levels of HbA1C and TC. 58 , 59 These findings suggest the successful establishment of the rabbit model replicating key features of DRN.\n\nDRN leads to retinal abnormalities that impair function before the onset of clinical DR, in some cases, even before diabetes is diagnosed. 17 , 60 In this study, a significant reduction in mean b‐wave amplitude was identified in the model rabbits ( p < 0.01), accompanied by a decrease in the amplitude of the OP wave (Figure 5 ). This reduction in amplitude strongly correlates with the extent of retinal damage, 5 suggesting delayed signal transmission in bipolar cells and Muller cell dysfunction. 61 These findings are consistent with previous studies involving streptozotocin‐induced diabetic rats and further support electrophysiological impairments as an early indicator of retinal neuropathy. 62 VEP provides an objective evaluation of visual system function. 53 In model rabbits, a significant reduction in mean P2 wave amplitudes ( p < 0.05) and a prolongation in P2 wave latency were observed (Figure 6 ), indicating optic nerve injury and disruption of the visual pathway. A decrease in amplitude combined with increased latency in VEP readings strongly suggests damage to the optic nerve. Miura 54 demonstrated that patients with diabetes mellitus may exhibit antecedent neuropathy despite the absence of clinically detectable ophthalmoscopic or morphological abnormalities. Moreover, VEP can detect such functional impairments before the appearance of visible changes during fundus examination. These findings are consistent with the results of this study. The present study represents the first assessment of visual impairment in DRN model rabbits using full‐field ERG and VEP recordings under scotopic and photopic conditions. The results suggest that early retinal dysfunction and retinopathy in DRN may initially manifest in the optic retina and central optic nerve.\n\nStructural analyses through SD‐OCT and H&E staining provided complementary perspectives on retinal alterations in early diabetic rabbits. SD‐OCT was performed on conscious animals to assess retinal and choroidal thickness in superior and inferior regions (Figure 7B ). At 9 weeks, diabetic rabbits exhibited no significant retinal thinning compared to controls (Table S1 ). These findings align with the observations in a diabetic mouse model, which demonstrate impairments in a‐wave, b‐wave, and OPs despite preserved inner retinal thickness. 63 This evidence underscores the suitability of the DRN rabbit model for studying early neural retinal pathology while highlighting the advantage of OCT in awake animals to reduce use and support animal welfare.\n\nIn contrast, H&E staining revealed marked retinal edema in diabetic animals, characterized by disorganized cellular distribution from the retinal nuclear layer to the ganglion cell layer, reduced intercellular spacing, and increased vacuolization (Figure 8 ). 64 , 65 Comparable disruptions have been observed in STZ‐induced diabetic rats, including alterations in GCL, INL, and ONL at 8 weeks 66 and vacuolar degeneration of ganglion cells at 4 weeks. 67 Notably, histologically measured retinal thickness was significantly greater than that obtained via OCT, likely due to inherent differences between in vivo imaging and ex vivo histological processing. In vivo OCT, despite its high‐resolution capabilities, may underestimate diffuse edema because its resolution and segmentation algorithms—primarily optimized for human retinal architecture—are not fully attuned to detect subtle, uniformly distributed changes, particularly in rabbit models with distinct retinal layer definitions. Conversely, H&E staining of ex vivo sections offers exquisite cellular and subcellular detail but is susceptible to processing artifacts, such as those arising from fixation, dehydration, and embedding, which can exaggerate tissue swelling. Consequently, the full‐thickness edema observed histologically likely reflects both genuine pathological alterations and artifacts introduced during tissue processing, whereas OCT yields a more conservative estimate of retinal thickness. Future research should aim to refine OCT segmentation protocols and develop species‐specific criteria to enhance the correlation between these imaging modalities.\n\nFurthermore, WF‐FFA and Optos UWF imaging revealed no vascular abnormalities or basement membrane thickening in the DRN model, with similar results between diabetic and control groups (Figure 7 ). Specifically, FFA is highly sensitive for detecting microvascular leakage, subtle perfusion defects, and early vascular abnormalities. By dynamically imaging the distribution of fluorescein dye in the retinal vasculature, FFA provides detailed visualization of vascular integrity, enabling the identification of even minor instances of leakage that might be missed by other modalities. 68 Although Ljubimov et al. 69 reported basement membrane thickening in diabetic retinopathy, such alterations were absent in our model. Notably, this study is the first to assess early DRN severity in rabbits using Optos UWF imaging, which, along with SD‐OCT, confirmed the presence of a well‐defined visual streak and clear optic bands in awake diabetic rabbits, supporting findings by Paulus et al. 70\n\nThis study identified pronounced glial activation and substantial neuronal loss in DRN retinas. This activation may intensify retinal damage by amplifying inflammatory signaling pathways, aligning with prior findings that associate glial activation with DRN. 71 , 72 Concurrently, the results revealed a marked reduction in ganglion and displaced amacrine cells within the GCL. Decreased RBPMS‐labeled ganglion cell density further supports the hypothesis that diabetic retinas undergo progressive neuronal loss, ultimately disrupting visual signaling.\n\nThis model effectively isolates early neurodegenerative events from subsequent microvascular pathology, establishing it as a valuable preclinical tool for investigating the mechanisms underlying DRN. Full‐field ERG and VEP emerged as highly sensitive screening tools, capable of detecting retinal nerve dysfunction before the onset of irreversible damage occurs. While early neuronal and glial alterations are evident in preclinical diabetes models, conventional diagnostic approaches typically identify neuropathy only during more advanced stages. Preclinical evidence indicates that retinal neuropathy, partially characterized by photoreceptor dysfunction, precedes overt vascular alterations, reinforcing the rationale for neuroprotective strategies to prevent or delay apoptotic neuronal cell death. These findings highlight the critical need for early detection and intervention targeting neurodegenerative processes in DR. In summary, this model elucidates the temporal progression of diabetic retinal alterations while emphasizing the therapeutic potential of early neuroprotective approaches to enhance clinical outcomes in individuals with diabetes.\n\nThis study has some limitations. First, using a rabbit model introduces physiological and anatomical disparities compared to humans, potentially limiting direct clinical applicability. Although the DRN model was successfully replicated, the short observation period restricted the comprehensive assessment of disease progression. Second, suboptimal housing conditions, including limited control over movement and dietary intake following induction, may have introduced confounding factors. Alloxan injection (80 mg/kg) yielded promising outcomes; however, the small sample size constrains statistical robustness and reproducibility. Future studies should employ larger cohorts and adopt a multidisciplinary strategy integrating in vitro, ex vivo, and clinical research to more precisely define the biological and pathophysiological mechanisms underlying DRN.\n\n— Source (discussion, peer-reviewed): Xinlu Li, Xiaojing Dong, Defei Feng, et al. · (2025) · \"Establishment of a novel alloxan‐induced rabbit model exhibiting unique diabetic retinal neuropathy features assessed via ERG + VEP\" · Animal Models and Experimental Medicine · doi: 10.1002/ame2.70032 · PMCID: PMC12710098 · PMID: 40536048\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12582910-conclusion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-conclusion", "source": "PubMed Central open-access full text", "pmcid": "PMC12582910", "pmid": "41184217", "doi": "10.1002/jfa2.70095", "title": "Using Nominal Group Technique to Gather Recommendations in the Decision‐Making for Amputation Due to Diabetes", "journal": "Journal of Foot and Ankle Research", "publication_year": 2025, "citation": "Emilee Kim Ming Ong, Carolyn Murray, Susan Hillier, et al. · (2025) · \"Using Nominal Group Technique to Gather Recommendations in the Decision‐Making for Amputation Due to Diabetes\" · Journal of Foot and Ankle Research · doi: 10.1002/jfa2.70095 · PMCID: PMC12582910 · PMID: 41184217", "question": "What does the published research conclude about \"Using Nominal Group Technique to Gather Recommendations in the Decision‐Making for Amputation Due to Diabetes\"? Cite a peer-reviewed source.", "answer": "The outcomes of this study are the first steps towards establishing evidence‐based guidelines for making decisions for amputation. A person‐centred approach is required when making decisions for non‐emergency amputation. This is achieved by a mutual understanding of goals and priorities, and differing meanings of quality of life through systems that enable continuity of health practitioners. Identifying the optimal time for amputation may be facilitated through early discussions. Further research into how these recommendations can be implemented into multi‐disciplinary clinics across different settings is now required.\n\n— Source (conclusions, peer-reviewed): Emilee Kim Ming Ong, Carolyn Murray, Susan Hillier, et al. · (2025) · \"Using Nominal Group Technique to Gather Recommendations in the Decision‐Making for Amputation Due to Diabetes\" · Journal of Foot and Ankle Research · doi: 10.1002/jfa2.70095 · PMCID: PMC12582910 · PMID: 41184217\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12890618-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC12890618", "pmid": "41684452", "doi": "10.3389/fendo.2025.1733840", "title": "Maintained diabetes remission among normal BMI individuals achieved without ongoing intervention: a three-year follow-up study of intermittent calorie restriction", "journal": "Frontiers in Endocrinology", "publication_year": 2026, "citation": "Ruiyu Wu, Xiao Yang, Xu Zhou, et al. · (2026) · \"Maintained diabetes remission among normal BMI individuals achieved without ongoing intervention: a three-year follow-up study of intermittent calorie restriction\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2025.1733840 · PMCID: PMC12890618 · PMID: 41684452", "question": "What did the discussion section of the paper \"Maintained diabetes remission among normal BMI individuals achieved without ongoing intervention: a three-year follow-up study of intermittent calorie restriction\" cover?", "answer": "This study demonstrates that diabetes remission achieved through a 3-month CMNT diet intervention can be maintained over 3 years without ongoing pharmacological or diet interventions. Notably, 64.7% (n = 17, of which 11 maintained remission) of participants in the CMNT group who had achieved remission by the 3rd-month post-intervention, maintained it for 3 years under ad libitum dietary conditions, highlighting the potential of this approach to alleviate the burden of long-term disease management. Different from previous studies, such as the DIRECT trial, which required ongoing support to mitigate weight regain and preserve remission, our findings underscore the feasibility of achieving long-term remission without structured maintenance strategies. Although this remission requires maintaining a normal BMI, the findings nonetheless challenge the conventional assumption that prolonged intervention is indispensable.\n\nLong-term weight maintenance interventions have been used to support long-term diabetes remission due to the effects of weight regain, but their outcomes remain suboptimal ( 13 ). In the DIRECT follow-up study, for instance, even with low-intensity rescue programs provided over three to five years, many participants experienced weight regain, leading to a decline in remission rates from 51% to 13% ( 7 ). The CMNT diet intervention resulted in weight loss, while weight regain was also observed and primarily among participants who achieved remission. However, relapse was less frequent, even though only general dietary recommendations was provided. Linear regression analysis further revealed that maintenance of remission was not affected by weight changes during the follow-up. In energy-restricted diets, weight loss and weight regain are common phenomena, including participants from CMNT. However, given that the baseline BMI of the CMNT group was not elevated (approximately 25 kg/m²) and further decreased following the intervention, the average BMI remained below 24 kg/m² even after weight regain. In DIRECT study, a significant proportion of the participants exhibited a BMI greater than 30 kg/m², and even subsequent to the intervention, the BMI remained greater than 27 kg/m² ( 7 ). This may provide a reason for the high diabetes remission rate observed in the three-year follow-up after CMNT intervention in this study.\n\nThe Dual-Cycle Hypothesis of T2DM suggests that the interaction between hepatic insulin resistance caused by liver fat accumulation and β-cell dysfunction induced by pancreatic exposure to hypertriglyceridemia drives the onset and progression of T2DM ( 14 ). Among participants in the CMNT group who maintained remission, the BMI was 23.9 kg/m² at baseline and 21.7 kg/m² after intervention. In the three newly added subjects whose diabetes was in remission, the intervention was followed by the use of only one hypoglycaemic agent and concomitant HbA1c of less than 6%. Although these participants’ weight had increased during the follow-up, all but one participant had a BMI below 25 kg/m²in the 3 -year follow-up. A BMI below 25 kg/m² is generally associated with a lower risk of developing T2DM and is often indicative of relatively limited hepatic fat accumulation ( 15 ). This phenotype may partly explain the favorable conditions that support diabetes remission maintenance in our cohort. However, this assumption requires further validation with direct measurements of hepatic steatosis, as the current study lacks corresponding liver fat data. Furthermore, the dietary recommendations stipulated within the Dietary Guidelines for Diabetes in China, which were to be adhered to by subjects during the follow-up period, including a low GL diet, management of staple foods, and increased vegetable intake, also demonstrated glycaemic control benefits. Overall, maintaining diabetes remission may be partly attributable to sustaining a normal BMI together with adherence to healthy dietary patterns.\n\nAs long as the pancreas can compensate by increasing insulin secretion, plasma glucose control can be maintained in both muscle and liver, even in the presence of insulin resistance ( 14 ). Some studies have demonstrated that in the absence of weight loss, such as in the context of intensive insulin therapy ( 16 ), GLP-1 therapy ( 17 ), or other interventions, diabetes remission can be achieved. In this follow-up study, we evaluated the impact of the CMNT diet intervention on participants’ use of insulinotropic agents and insulin. Results showed a 86.7% reduction in usage ( Supplementary Table 6 ) among participants in the CMNT group during the intervention period, with no subsequent increase observed throughout the follow-up period. These findings may reflect an improvement in the participants’ endogenous insulin secretory capacity, potentially reducing their reliance on insulin-secretagogue medications or exogenous insulin therapy. Furthermore, animal studies have demonstrated that CMNT can promote β-cell proliferation and enhance insulin secretion in mice, supporting a possible mechanistic basis for the observed clinical benefits ( 18 ). In addition, we observed that participants in the CMNT group who remained in remission in the 3-year follow-up exhibited higher HOMA-β levels compared with those who did not ( Figure 2C ). Although this observation is based on a relatively small sample size and requires confirmation in larger and more rigorous studies, it remains a noteworthy finding. Taken together, these observations may indicate a potential role of CMNT in supporting metabolic improvements that favor diabetes remission, possibly through modest enhancements in endogenous insulin secretion and β-cell function.\n\nThe majority of individuals with diabetes express a strong desire to achieve autonomy to live their lives as they choose, free from the need for medication, insulin, or restrictive diets, and without the requirement for strenuous exercise ( 19 , 20 ). This is a goal that their physicians had previously indicated unattainable, even if medication was ceased, particularly in individuals dependent on insulin ( 11 , 21 ). Nevertheless, the necessity of long-term disease management imposes varying degrees of psychological stress on patients ( 22 ). In this study, those who achieved remission in CMNT group were not only free from the need for antidiabetic medications, but also did not require interventions that differed from their normal routine. These benefits were reflected in the markedly superior quality of life in the CMNT group in comparison to the control group. Diabetes-related complications are common and can impact multiple organ systems, leading to increased mortality, blindness and renal failure ( 23 ). Despite the absence of ongoing intervention during the 3-year follow-up period, the CMNT group exhibited a five-fold reduction in hospitalisation rates and a three-fold reduction in complication rates compared to the control group ( Supplementary Table 7 ). In summary, CMNT-induced remission could enable some individuals to reduce their reliance on pharmacological therapy and may be associated with improvements in disease-related burden, although further studies are needed to confirm long-term effects without ongoing intervention.\n\nIt is important to acknowledge the limitations of this study. On the one hand, the sample size was relatively small, and the three-year follow-up period was not sufficiently long. Future research with larger cohorts and longer follow-up duration is needed to confirm these results and further explore the long-term impact of CMNT interventions on diabetes remission. On the other hand, CMNT needs to be validated for its effectiveness in remission diabetes in people with higher BMI, and its long-term benefits need to be explored. It should also be noted that remission status in the present study was defined solely on the basis of annual HbA1c measurements and thus reflects the remission status only at the time of assessment. Owing to the absence of additional day-to-day normoglycaemic data, the findings do not provide evidence for sustained metabolic stability.\n\nIn conclusion, this study highlights the CMNT diet as a promising intervention for achieving long-term diabetes remission. It is noteworthy that this remission was maintained without the requirement for ongoing pharmacological or dietary intervention, provided that a normal BMI was preserved. Meanwhile, the preservation of pancreatic β-cell function is also an important contributing factor. This diet-focused approach demonstrates the potential to reduce reliance on insulin and insulinotropic agents while improving quality of life and minimizing the burden of long-term management.\n\n— Source (discussion, peer-reviewed): Ruiyu Wu, Xiao Yang, Xu Zhou, et al. · (2026) · \"Maintained diabetes remission among normal BMI individuals achieved without ongoing intervention: a three-year follow-up study of intermittent calorie restriction\" · Frontiers in Endocrinology · doi: 10.3389/fendo.2025.1733840 · PMCID: PMC12890618 · PMID: 41684452\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-9695880-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC9695880", "pmid": "36432557", "doi": "10.3390/nu14224870", "title": "Investigating the Effectiveness of Very Low-Calorie Diets and Low-Fat Vegan Diets on Weight and Glycemic Markers in Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis", "journal": "Nutrients", "publication_year": 2022, "citation": "Anjali Kashyap, Alexander Mackay, Ben Carter, et al. · (2022) · \"Investigating the Effectiveness of Very Low-Calorie Diets and Low-Fat Vegan Diets on Weight and Glycemic Markers in Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis\" · Nutrients · doi: 10.3390/nu14224870 · PMCID: PMC9695880 · PMID: 36432557", "question": "What is the published background on \"Investigating the Effectiveness of Very Low-Calorie Diets and Low-Fat Vegan Diets on Weight and Glycemic Markers in Type 2 Diabetes…\"? Cite a peer-reviewed source.", "answer": "Type 2 Diabetes Mellitus (T2DM) is a global epidemic, driven by an increased prevalence of obesity in both children and adults [ 1 ]. Increased consumption of calorific foods including processed foods and beverages, meat and other animal products, sugary beverages, and refined grains are believed to play a key role in the growing rates of T2DM worldwide [ 2 ]. The International Diabetes Federation estimate that approximately 537 million adults (20–79 years) are living with diabetes. The total number of people living with diabetes is projected to rise to 643 million by 2030 and 783 million by 2045 [ 3 ], with the predominant type being T2DM. With fewer than 2% of people with T2DM entering a state of spontaneous remission [ 4 ], the present clinical paradigm is that T2DM is an irreversible condition.\n\nThe primary approach for management of T2DM is to achieve and maintain weight loss [ 5 ]. Evidence has shown a multifactorial intervention in the form of caloric restriction, exercise, and behavior change has optimal effects in improving glycemic control and weight [ 6 , 7 ]. Current dietary interventions for the management of T2DM include restricting carbohydrates, cholesterol, and fat intake, as well as caloric restriction [ 8 ]. Dietary restriction therapies for management and cessation of T2DM have mainly focused on weight loss through the implementation of either low-calorie diets (LCD) defined as 1200–1500 kcal/day [ 9 , 10 , 11 ] or very low-calorie diets (VLCD) ranging from 450–800 kcals/day [ 12 ]. Current literature supports VLCD diets, illustrating that such diets are superior in inducing/promoting rapid weight reductions, improving insulin secretion, and lowering hemoglobin A1c (HbA1c) to levels seen in pre-diabetes or normoglycemia [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ].\n\nPlant-based diets, focusing on inclusion of foods from plant sources and exclusion of animal-based products, have gained recognition in public heath for not only their potential in promoting sustainability, but also to curb the onset and assist in management of chronic disease [ 23 ], including cardiovascular disease, some cancers, and T2DM [ 24 , 25 , 26 , 27 ]. Clinical studies have demonstrated improvements in glycemic control, blood lipids and body weight. In some cases, this has been achieved to a greater degree than conventional dietary interventions [ 28 ]. Proposed mechanisms for this have been attributed to increased consumption of plant foods (naturally rich in minerals, vitamins, and antioxidants) and reduced intake of processed and red meats [ 29 , 30 , 31 ]. A study conducted to determine the nutritional adequacy of a low-fat vegan diet concluded that vegan diets have positive impacts on energy and plasma lipids [ 32 ]. The lipid lowering effects of plant-based diets can be attributed to negligible dietary cholesterol intake, reduced saturated fat content and cholesterol-lowering effects of soluble fiber [ 33 ]. These effects are important, as cardiovascular complications are one of the leading causes of worldwide morbidity and mortality in patients with T2DM.\n\nA recently published systematic review and meta-analysis [ 34 ] confirmed that the consumption of vegan diets yields favorable results in some cardiometabolic health measures in overweight patients and those with T2DM. Despite there being an overlap in review content, our review is unique for several reasons: the most important being the current focus on patients with diabetes and the inclusion of VLCD diets. We included a side-by-side analysis by looking at both vegan and VLCD diets, being current popular approaches. Our inclusion criteria did not include individuals with pre-diabetes, but included studies of any length of intervention period, to facilitate a broader analysis for clinical relevance. This approach means that these results are translatable for patients, clinicians, and healthcare workers with an interest in dietary approaches to manage with type 2 diabetes and body weight control.\n\nOur study assessed the evidence available to support very low-calorie diets (VLCD) and vegan diets for management of body weight and/glycemic control in patients with T2DM.\n\n— Source (introduction, peer-reviewed): Anjali Kashyap, Alexander Mackay, Ben Carter, et al. · (2022) · \"Investigating the Effectiveness of Very Low-Calorie Diets and Low-Fat Vegan Diets on Weight and Glycemic Markers in Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis\" · Nutrients · doi: 10.3390/nu14224870 · PMCID: PMC9695880 · PMID: 36432557\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12733237-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12733237", "pmid": "41465463", "doi": "10.3390/ijms262412034", "title": "Dapagliflozin Preserves Peripheral Nerve Structure and Reduces Neuropathic Damage in Streptozotocin-Induced Diabetic Peripheral Neuropathy", "journal": "International Journal of Molecular Sciences", "publication_year": 2025, "citation": "Anca-Maria Țucă, Alexandra Nicoleta Preda, Georgică Târtea, et al. · (2025) · \"Dapagliflozin Preserves Peripheral Nerve Structure and Reduces Neuropathic Damage in Streptozotocin-Induced Diabetic Peripheral Neuropathy\" · International Journal of Molecular Sciences · doi: 10.3390/ijms262412034 · PMCID: PMC12733237 · PMID: 41465463", "question": "What is the published background on \"Dapagliflozin Preserves Peripheral Nerve Structure and Reduces Neuropathic Damage in Streptozotocin-Induced Diabetic Peripheral Neuropathy\"? Cite a peer-reviewed source.", "answer": "Diabetes mellitus (DM) is a chronic metabolic disease characterized by persistent hyperglycemia and impaired pancreatic β-cell function and/or insulin resistance, with systemic consequences at the vascular, renal, hepatic, and nervous levels [ 1 ]. In recent years, the global prevalence of diabetes has continued to increase, a situation that amplifies the burden of associated complications, including nephropathy, retinopathy, neuropathy, and cardiovascular disease [ 2 , 3 ].\n\nThe experimental model of diabetes induced by STZ administration in mice is widely used to investigate the pathological mechanisms related to β-cell destruction and secondary hyperglycemia. STZ is a cytotoxic agent with affinity for β-cells, which generates necrosis and insulin dysfunction, thus gradually generating a model of type 1 or “cytotoxic” type diabetes, depending on the scheme (dose, number of injections) [ 4 , 5 ]. Furthermore, this model allows for the assessment of metabolic, oxidative–inflammatory, and apoptotic changes induced by hyperglycemia, in addition to testing therapeutic strategies with translational potential [ 5 ].\n\nIn this paradigm, inhibitors of the sodium–glucose cotransporter 2 (SGLT2) have attracted considerable attention. Dapagliflozin, one such SGLT2 inhibitor, has been approved for clinical therapy of type 2 diabetes, with effects on blood glucose lowering, body weight reduction, and cardiovascular and renal protection [ 6 , 7 , 8 ]. Furthermore, recent experimental data suggest that dapagliflozin may exert beneficial effects beyond glucose metabolism, including reducing oxidative stress, inflammation, fibrogenesis, and apoptosis in diabetic target organs [ 9 , 10 , 11 , 12 ]. Building on these observations, the glucose-independent actions of dapagliflozin appear to be mediated through several interconnected molecular pathways, including activation of the AMPK/SIRT1 pathway, leading to improved mitochondrial function and reduced ROS production; inhibition of NF-κB signaling and downstream pro-inflammatory cytokines; attenuation of TGF-β-mediated fibrogenic pathways; and modulation of apoptotic balance by decreasing pro-apoptotic markers (e.g., Bax) and enhancing anti-apoptotic signaling (e.g., Bcl-2) [ 9 , 10 , 11 , 12 ].\n\nIn the context of the STZ model, preclinical studies have demonstrated that dapagliflozin administered to diabetic mice or rats can ameliorate renal, cardiac, or hepatic damage through mechanisms involving activation of the 5’ AMP-activated protein kinase (AMPK) pathway, inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), reductions in reactive oxygen species formation, and improvements in mitochondrial dysfunction [ 13 , 14 , 15 ].\n\nDespite the progress made, the extension of the beneficial effects of dapagliflozin on metabolic, oxidative, and apoptotic parameters in an experimental model of STZ-induced diabetes in mice remains unclear. In addition, in the current literature, a “classical” preclinical study (in diabetic rats/mice) evaluating dapagliflozin directly on diabetic peripheral neuropathy (DPN) with standard neuropathy endpoints (nerve conduction, intraepidermal fiber density, hyperalgesia, etc.) is lacking. The evidence in this regard is not yet robust and generalized.\n\nLarge, long-term clinical trials with a primary hypothesis of “neuropathy” are still limited. In clinical practice, the treatment of diabetic neuropathy remains focused on glycemic control, risk factor control (hypertension, dyslipidemia), symptom relief (pain, paresthesia), and not necessarily on proven disease modifiers, agents improving long-term disease outcomes [ 16 , 17 , 18 ].\n\nTherefore, the present study aims to investigate the effects of dapagliflozin administration in STZ-induced diabetic mice on glycemic control, clinical profile, oxidative stress, behavioral changes, and possible histopathological changes in peripheral neuropathy.\n\n— Source (introduction, peer-reviewed): Anca-Maria Țucă, Alexandra Nicoleta Preda, Georgică Târtea, et al. · (2025) · \"Dapagliflozin Preserves Peripheral Nerve Structure and Reduces Neuropathic Damage in Streptozotocin-Induced Diabetic Peripheral Neuropathy\" · International Journal of Molecular Sciences · doi: 10.3390/ijms262412034 · PMCID: PMC12733237 · PMID: 41465463\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12941053-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12941053", "pmid": "41753934", "doi": "10.3390/healthcare14040420", "title": "Psychological Aspects and Implications of Food Addiction and Glucose Control in Type 2 Diabetes: A Pilot Mixed-Methods Study", "journal": "Healthcare", "publication_year": 2026, "citation": "David J. Johnson, Laura A. Buchanan, Erin M. Saner, et al. · (2026) · \"Psychological Aspects and Implications of Food Addiction and Glucose Control in Type 2 Diabetes: A Pilot Mixed-Methods Study\" · Healthcare · doi: 10.3390/healthcare14040420 · PMCID: PMC12941053 · PMID: 41753934", "question": "What is the published background on \"Psychological Aspects and Implications of Food Addiction and Glucose Control in Type 2 Diabetes: A Pilot Mixed-Methods Study\"? Cite a peer-reviewed source.", "answer": "As of 2021, the Centers for Disease Control estimated that more than 38 million people in the United States were living with diabetes and over 97 million with prediabetes, underscoring the scale of dysglycemia as a public health challenge [ 1 ]. Type 2 Diabetes (T2D) management hinges on daily self-care behaviors, dietary choices, physical activity, medication use, and glucose monitoring, yet many individuals struggle to translate education into sustained behavior change [ 2 ]. Dysregulated eating, emotional eating, and loss of control around highly processed foods are strongly correlated with T2D [ 3 ].\n\nIn the face of the growing epidemic of diabetes, the introduction of continuous glucose monitors (CGMs) has changed how these patients view the direct relationship between their food intake and subsequent glucose readings [ 4 ]. Food addiction (FA) has emerged as a construct capturing compulsive, addictive-like responses to ultra-processed foods rich in refined carbohydrates and fats [ 5 ]. Population data indicates that prevalence of FA as measured by the modified Yale Food Addiction Scale (mYFAS) affects approximately 20% of adults, and with rates as high as 30% in T2D [ 6 ]. Although the FAconstruct remains an area of active debate, symptom-based measures such as the mYFAS 2.0 offer a pragmatic way to examine addictive-like eating behaviors relevant to diabetes self-management. FA symptoms, including cravings, diminished control, and continued overeating despite negative consequences, are associated with higher BMI, binge-eating pathology, and metabolic risk, and may help explain why some individuals experience disproportionate difficulty adhering to standard dietary recommendations [ 3 , 5 , 6 ]. Identifying and targeting FA-related mechanisms in T2D could therefore offer novel pathways to improving both behavioral adherence and glycemic outcomes.\n\nCGMs have transformed how people with diabetes perceive the relationship between their daily choices and glucose fluctuations. Real-time continuous glucose monitoring systems provide near-continuous glycemic data, visual trend arrows, and summary metrics (e.g., time-in-range, glycemic variability) that can be used to guide both pharmacologic adjustments and lifestyle decisions [ 4 , 7 ]. Professional societies now recommend CGMs for selected adults with T2D to improve glycemic control and reduce hypoglycemia [ 8 , 9 , 10 , 11 ]. Recent qualitative and mixed-method studies in adults with T2D report that CGM can increase motivation, confidence in self-management, and perceived control by making glucose responses to meals and activities more visible and personally meaningful [ 12 , 13 , 14 , 15 , 16 ].\n\nBeyond biomedical utility, CGMs can be conceptualized as a behavioral feedback tool embedded within self-regulation frameworks. Self-regulation and feedback-control frameworks propose that timely, interpretable feedback strengthens the perceived connection between behavior and physiological outcomes, thereby supporting self-monitoring and reinforcing adaptive health behaviors [ 17 , 18 ]. Early work has suggested that CGM-guided behavioral education and intermittent CGM use may prompt dietary modifications, increase awareness of physiological responses, and facilitate problem solving around glycemic excursions [ 19 , 20 , 21 , 22 ].\n\nParallel advances in digital health services offer additional context. Mobile health apps, Short Message Service (SMS)-based programs, and wearable activity trackers have been shown to improve self-management behaviors, self-efficacy, and in some cases glycemic outcomes in T2D by providing real-time or near-real-time feedback, goal tracking, and prompts [ 23 , 24 , 25 , 26 , 27 ]. For example, diabetes self-management apps and text-messaging interventions have improved hemoglobin A1c (HbA1c) and self-care behaviors by combining monitoring with tailored feedback and coaching [ 23 , 24 ]. Wearable activity trackers similarly leverage immediate feedback, self-monitoring, and goal setting to increase physical activity and support metabolic health that have explicitly examined how CGM, as a glucose-specific feedback modality, may influence addictive-like eating among adults with T2D [ 25 , 26 ].\n\nThe present mixed-methods study examines how CGM, when integrated into a structured group medical visit (GMV) program, may act as a feedback mechanism that strengthens awareness, accountability, and motivation around dietary behavior in adults with T2D. We assess changes in glycemic outcomes, patient activation, and FA symptoms (using the modified Yale Food Addiction Scale 2.0) and integrate these quantitative improvements with participants’ qualitative accounts of CGM-supported behavior change. By focusing on adults with T2D engaged in CGM-supported GMVs, this study aims to generate preliminary evidence on CGM’s potential to function as a behavioral intervention targeting both metabolic control and addictive-like eating.\n\n— Source (introduction, peer-reviewed): David J. Johnson, Laura A. Buchanan, Erin M. Saner, et al. · (2026) · \"Psychological Aspects and Implications of Food Addiction and Glucose Control in Type 2 Diabetes: A Pilot Mixed-Methods Study\" · Healthcare · doi: 10.3390/healthcare14040420 · PMCID: PMC12941053 · PMID: 41753934\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13021413-conclusion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-conclusion", "source": "PubMed Central open-access full text", "pmcid": "PMC13021413", "pmid": "41908910", "doi": "10.3389/fcdhc.2026.1708124", "title": "Continuous glucose monitoring, diabetes distress, and well-being in adults with type 1 diabetes: findings from a National Survey in Lithuania", "journal": "Frontiers in Clinical Diabetes and Healthcare", "publication_year": 2026, "citation": "Jurga Šuminienė, Rimantas Stukas, Virginija Gaigalaite, et al. · (2026) · \"Continuous glucose monitoring, diabetes distress, and well-being in adults with type 1 diabetes: findings from a National Survey in Lithuania\" · Frontiers in Clinical Diabetes and Healthcare · doi: 10.3389/fcdhc.2026.1708124 · PMCID: PMC13021413 · PMID: 41908910", "question": "What does the published research conclude about \"Continuous glucose monitoring, diabetes distress, and well-being in adults with type 1 diabetes: findings from a National Survey in…\"? Cite a peer-reviewed source.", "answer": "In this national survey of adults with type 1 diabetes in Lithuania, CGM use was associated with lower diabetes distress and higher hypoglycemia confidence compared with flash glucose monitoring. CGM was not independently associated with good general well-being after adjustment, suggesting that observed associations may operate indirectly through glycemic stability and hypoglycemia-related emotional factors. Associations appeared more pronounced in selected higher-risk subgroups; however, given the cross-sectional design and exploratory subgroup analyses, these findings should be interpreted cautiously. Longitudinal studies are needed to clarify temporal relationships and potential causal pathways.\n\nOverall, the results support consideration of CGM as part of comprehensive, patient-centered diabetes care frameworks, particularly for individuals at elevated psychosocial vulnerability.\n\n— Source (conclusions, peer-reviewed): Jurga Šuminienė, Rimantas Stukas, Virginija Gaigalaite, et al. · (2026) · \"Continuous glucose monitoring, diabetes distress, and well-being in adults with type 1 diabetes: findings from a National Survey in Lithuania\" · Frontiers in Clinical Diabetes and Healthcare · doi: 10.3389/fcdhc.2026.1708124 · PMCID: PMC13021413 · PMID: 41908910\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12831128-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12831128", "pmid": "41583544", "doi": "10.1155/bmri/3230665", "title": "Awareness of Vital Complications and Associated Factors Among Type 2 Diabetic Patients in Al‐Hudaydah, Yemen: A Cross‐Sectional Study", "journal": "BioMed Research International", "publication_year": 2026, "citation": "Khaled Alselwy, Mogeeb Saeed · (2026) · \"Awareness of Vital Complications and Associated Factors Among Type 2 Diabetic Patients in Al‐Hudaydah, Yemen: A Cross‐Sectional Study\" · BioMed Research International · doi: 10.1155/bmri/3230665 · PMCID: PMC12831128 · PMID: 41583544", "question": "What is the published background on \"Awareness of Vital Complications and Associated Factors Among Type 2 Diabetic Patients in Al‐Hudaydah, Yemen: A Cross‐Sectional Study\"? Cite a peer-reviewed source.", "answer": "Diabetes mellitus (DM) is a chronic inflammatory disease that leads to severe and even fatal complications. It is a significant public health challenge in Yemen, with a mortality rate of 15.42 per 100,000 people in 2020, ranking Yemen 120th globally for diabetes‐related mortality [ 1 ]. Common complications of Type 2 diabetes mellitus (T2DM) include diabetic nephropathy, acute coronary syndrome, retinopathy leading to vision impairment, cataracts, and myocardial infarction. These complications often develop gradually during the undiagnosed period preceding diagnosis owing to the inability of the body to control the disease process properly [ 2 – 7 ].\n\nAwareness and early detection of diabetic complications are vital to reduce this alarming burden. Previous studies in Yemen have reported low awareness among T2DM patients regarding potential complications, especially cardiovascular risks [ 8 – 10 ]. Understanding hypoglycemia symptoms can vary depending on individual treatment regimens and health literacy levels [ 11 , 12 ]. This study is aimed at assessing the awareness of diabetes complications, especially retinopathy, nephropathy, and hypoglycemia symptoms, and associated factors among patients with T2DM attending state‐run hospitals and clinics in Al‐Hudaydah, Yemen. The primary goal is to help reduce diabetes‐related morbidity and mortality in the country by improving patient awareness and guiding targeted educational programs.\n\n— Source (introduction, peer-reviewed): Khaled Alselwy, Mogeeb Saeed · (2026) · \"Awareness of Vital Complications and Associated Factors Among Type 2 Diabetic Patients in Al‐Hudaydah, Yemen: A Cross‐Sectional Study\" · BioMed Research International · doi: 10.1155/bmri/3230665 · PMCID: PMC12831128 · PMID: 41583544\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13043021-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC13043021", "pmid": "40562360", "doi": "10.1016/j.eprac.2025.05.751", "title": "Continuous Glucose Monitoring–Guided Insulin Infusion in Critically Ill Patients Promotes Safety, Improves Time Efficiency, and Enhances Provider Satisfaction", "journal": "Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists", "publication_year": 2025, "citation": "Erin R. Giovannetti, Rachael O. Lee, Robert L. Thomas, et al. · (2025) · \"Continuous Glucose Monitoring–Guided Insulin Infusion in Critically Ill Patients Promotes Safety, Improves Time Efficiency, and Enhances Provider Satisfaction\" · Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · doi: 10.1016/j.eprac.2025.05.751 · PMCID: PMC13043021 · PMID: 40562360", "question": "What did the discussion section of the paper \"Continuous Glucose Monitoring–Guided Insulin Infusion in Critically Ill Patients Promotes Safety, Improves Time Efficiency, and Enhances Provider Satisfaction\" cover?", "answer": "The integration of rtCGM into critical care settings, particularly for ICU patients on insulin infusions, offers significant benefits. Our study demonstrates that rtCGM, when used in real-world settings with ongoing clinician validation and an IICC, provides high accuracy glucose measurements and maintains patient safety with low hypoglycemia rates. Specifically, just 0.2% of matched CGM and POC glucose values were <70 mg/dL, and we observed a 0.5% time below 70 mg/dL and 0.1% time below 54 mg/dL based on CGM metrics. Severe hypoglycemia remains a major concern in intensive insulin therapy due to its association with increased mortality and adverse neurological outcomes. Traditional blood glucose monitoring, which relies on intermittent POC measurements, may miss critical glucose fluctuations, leading to delayed detection of both hypo- and hyperglycemia. By providing continuous glucose data along with alarm capabilities, rtCGM enables earlier intervention and a more proactive approach to glucose management. Our protocol, in which a POC test was performed when glucose levels fell below 100 mg/dL, ensured timely confirmation and intervention, and further enhanced patient safety. Our findings align with previous studies supporting the safe use of rtCGM in critically ill patients, including those with shock, edema, and ECMO. 9 , 21\n\nThe low MARD of 12.5% between CGM and POC measurements, with 99.6% within zone A and B of the consensus error grid, further underscores the reliability of rtCGM in the ICU settings. While other studies have reported MARD values of 13.2% 21 and 13.9% 9 using a hybrid POC-CGM protocol for titration of an insulin infusion, our study is the first to show improved accuracy using the Dexcom G7 sensor. Another key advantage of rtCGM is its significantly faster TAT compared to POC glucose testing. While POC testing takes an average of nearly 5 minutes, rtCGM provides glucose readings in 3 seconds, offering substantial time savings ( Fig. 4 ). Over a 12-hour nursing shift, this could save an estimated 50 minutes, allowing more time for other critical patient care tasks. The reduction in manual glucose testing not only enhances efficiency but also reduces the burden on ICU staff, supporting overall workflow improvements.\n\nIn our study, critical care nurses reported high satisfaction with rtCGM implementation, citing reduced workload, improved efficiency, and perceived patient safety as key benefits. Additionally, rtCGM alarm capabilities and glucose trend arrows facilitated earlier recognition of impending hypoglycemia, allowing clinicians to intervene before critical glucose thresholds were reached. Given that ICU clinical decisions rely heavily on continuous physiologic monitoring, rtCGM has the potential to function as a vital sign itself, providing continuous glucose data rather than intermittent glycemic snapshots. This more proactive approach to glycemic monitoring and management could not only improve glycemic outcomes but may also help optimize resource utilization by reducing the frequency of POC testing and manual insulin adjustments. As a result, CGM-guided protocols have the potential to lower overall health care costs while enhancing patient safety.\n\nWe acknowledge the small sample size ( N = 35) and single-site, retrospective design limits the generalizability of our findings. However, we were encouraged by the diversity of our study population, including 45% non-White participants. Despite this strength, limitations in statistical power and demographic breadth should be considered when interpreting the results. While our study demonstrates potential benefits of CGM, there are areas that warrant further exploration. First, future studies should explore the optimal calibration strategies for CGM use in critically ill populations, as recent studies suggest that calibration frequency may impact MARD and SDRD in highly dynamic glucose environments. 22 , 23 Additionally, further research is needed to refine hospital-wide CGM-driven protocols, particularly in integrating rtCGM into the EHR for streamlined workflow implementation. Studies by Finn et al 24 and Lee et al 5 have demonstrated the feasibility of CGM policies following hospital-wide EHR integration across acuity levels. Investigating these factors will be essential to refining CGM as a clinical parameter and maximizing its impact on patient outcomes.\n\nIn conclusion, integrating rtCGM into the management of ICU patients on insulin infusions provides a promising strategy for enhancing patient safety, improving clinical outcomes, and reducing clinician workload. The combination of real-time glucose data and algorithm-driven insulin dosing offers an effective, efficient approach to managing glycemic variability in critically ill patients. By mitigating hypoglycemia risk, improving glycemic stability, and reducing the burden of frequent glucose monitoring, rtCGM has the potential to transform ICU glycemic management. As hospitals increasingly adopt digital health innovations, future research should focus on validating CGM-driven protocols, training clinician teams on CGM workflows, investigating rtCGM as a safety-net for prompting clinically significant unscheduled POC checks, and assessing the longitudinal impact of CGM implementation on morbidity and mortality in critically ill populations.\n\n— Source (discussion, peer-reviewed): Erin R. Giovannetti, Rachael O. Lee, Robert L. Thomas, et al. · (2025) · \"Continuous Glucose Monitoring–Guided Insulin Infusion in Critically Ill Patients Promotes Safety, Improves Time Efficiency, and Enhances Provider Satisfaction\" · Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · doi: 10.1016/j.eprac.2025.05.751 · PMCID: PMC13043021 · PMID: 40562360\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-13133891-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC13133891", "pmid": "42080080", "doi": "10.7150/ijms.131188", "title": "Potential influence of carbonic anhydrase 9 genetic variants and expression levels on the progression of diabetic retinopathy", "journal": "International Journal of Medical Sciences", "publication_year": 2026, "citation": "I-Chia Liang, Hsiang-Wen Chien, Kai Wang, et al. · (2026) · \"Potential influence of carbonic anhydrase 9 genetic variants and expression levels on the progression of diabetic retinopathy\" · International Journal of Medical Sciences · doi: 10.7150/ijms.131188 · PMCID: PMC13133891 · PMID: 42080080", "question": "Summarize the abstract of the paper titled \"Potential influence of carbonic anhydrase 9 genetic variants and expression levels on the progression of diabetic retinopathy\".", "answer": "Diabetic retinopathy (DR) represents one of the most common microvascular complications of diabetes, and proliferative diabetic retinopathy (PDR) is the most vision-threatening form. Carbonic anhydrase IX (CA9), a hypoxia-inducible enzyme, has been implicated in several pathological processes, but its involvement in DR has not been clarified. In this study, three CA9 single nucleotide polymorphisms (rs3829078, rs2071676, and rs1048638) were genotyped in diabetic patients with and without DR. Clinical characteristics were compared between groups, and expression analyses were conducted using public databases and ARPE-19 cells under hyperglycemic and hypoxic conditions. No significant association was observed between CA9 variants and DR susceptibility in the overall cohort. However, among patients aged ≤60 years, carriers of the rs1048638 C/A and C/A + A/A genotypes exhibited a significantly increased risk of PDR. Expression quantitative trait locus (eQTL) data from the GTEx database revealed higher CA9 mRNA expression in tissues harboring the rs1048638 A allele. Moreover, both transcriptomic data and in vitro experiments demonstrated upregulation of CA9 in ARPE-19 cells exposed to high glucose and hypoxia. These findings suggest that the rs1048638 polymorphism may modulate CA9 expression and contribute to PDR development in younger diabetic patients through hypoxia- and glucose-related mechanisms. Collectively, our findings suggest that CA9 may serve as a potential risk biomarker associated with the progression of DR, particularly in younger patients.\n\n— Source (abstract, peer-reviewed): I-Chia Liang, Hsiang-Wen Chien, Kai Wang, et al. · (2026) · \"Potential influence of carbonic anhydrase 9 genetic variants and expression levels on the progression of diabetic retinopathy\" · International Journal of Medical Sciences · doi: 10.7150/ijms.131188 · PMCID: PMC13133891 · PMID: 42080080\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12582623-discussion", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-discussion", "source": "PubMed Central open-access full text", "pmcid": "PMC12582623", "pmid": "41123059", "doi": "10.1097/HJH.0000000000004126", "title": "Arterial stiffness is associated with small and large fiber neuropathy: The Maastricht Study", "journal": "Journal of Hypertension", "publication_year": 2025, "citation": "Chidera Okoro, Carla J.H. van der Kallen, Sara B.A. Mokhtar, et al. · (2025) · \"Arterial stiffness is associated with small and large fiber neuropathy: The Maastricht Study\" · Journal of Hypertension · doi: 10.1097/HJH.0000000000004126 · PMCID: PMC12582623 · PMID: 41123059", "question": "What did the discussion section of the paper \"Arterial stiffness is associated with small and large fiber neuropathy: The Maastricht Study\" cover?", "answer": "This population-based study has two main findings. First, greater arterial stiffness, as determined by cfPWV, was significantly associated with lower small nerve fiber thickness and function, as shown by the lower composite Z scores for retinal nerve layer thickness, retinal sensitivity, and corneal nerve measures. Second, greater arterial stiffness was significantly associated with impaired large nerve fiber function, as shown by lower composite Z scores for peripheral nerve conduction velocities and lower Z scores for tibial nerve amplitude, along with a higher Z score for peripheral vibration perception thresholds. Importantly, these associations were independent of confounders, such as diabetes, hypertension, renal insufficiency, and prior cardiovascular disease. The strength of these associations was that each SD greater arterial stiffness was equivalent to approximately 1–5 years of additional aging in nerve functioning and structure, respectively.\n\nTo our knowledge, this is the first large population-based study to demonstrate that arterial stiffness is consistently associated with both ocular (small) and peripheral (large) fiber neuropathies. Specifically, our findings showed significant associations between arterial stiffness and individual components of retinal nerve layer thickness, retinal sensitivity, corneal nerve measures, peripheral nerve conduction velocities, amplitudes, and peripheral vibration perception thresholds. These findings provide new insights into the potential link between arterial stiffness and neuropathic process of both small and large nerve fibers.\n\nOur findings are consistent with those of previous studies [ 10 – 13 , 27 – 29 ], suggesting a relationship between arterial stiffness and neuropathy. However, these studies were either relatively small [ 10 – 13 ] or did not use cfPWV [ 15 , 27 ]. Huang et al. [ 15 ] found no association between arterial stiffness and retinal neuropathy in a large population-based study. However, arterial stiffness was calculated as the arterial stiffness index using pulse waveforms from the finger, which has only been moderately correlated with cfPWV [ 30 ]. This may explain the contrasting results from the present study, as we used cfPWV, which is widely regarded as the gold standard [ 14 ] for evaluating arterial stiffness.\n\nWe observed that greater arterial stiffness was associated with lower composite scores for retinal, corneal, and peripheral nerve functions. The advantage of using composite scores is that the impact of technical and biological variability is reduced. Importantly, associations with the individual components of the scores showed directionally similar results (Table S5).\n\nThe mechanisms linking arterial stiffness and neuropathy remain incompletely understood. A plausible explanation involves microvascular dysfunction, which may arise due to mechanical stress exerted by increased pulsatile energy on endothelial cells [ 31 ]. Endothelial dysfunction involves impaired regulation of vasodilation and vasoconstriction as well as impairment of antithrombotic and anti-inflammatory properties, setting the stage [ 32 ] for a chronic inflammatory response [ 33 , 34 ], creating a self-perpetuating cycle that further exacerbates endothelial dysfunction. Additionally, localized thrombosis within the microcirculation [ 35 ] may obstruct blood flow, leading to inadequate nutrient delivery to the nerves while simultaneously promoting heightened permeability of adjacent blood vessels. The latter, in turn, may allow infiltration of inflammatory cells and molecules into nerve tissue. Interestingly, we found that greater arterial stiffness was associated with lower peripheral nerve conduction velocities but was only partially associated with lower peripheral nerve amplitudes. This may be because the process of demyelination (i.e. lower peripheral NCV) occurs first, while axonal loss (i.e. lower peripheral nerve amplitude) manifests at a more advanced stage, as has been reported in previous studies [ 36 , 37 ].\n\nOur findings have clinical implications. The observed associations between greater arterial stiffness and both small-fiber and large-fiber neuropathy highlight the importance of vascular health in patients with neuropathy. Clinicians may consider testing for neuropathy in patients with worse cardiovascular health and, conversely, optimize cardiovascular risk management when treating patients with established neuropathy. Further interventional research is needed to investigate whether such interventions are beneficial.\n\nOur study has several strengths. First, the inclusion of a large population-based cohort, notably oversampled for individuals with type 2 diabetes, allowed us to investigate our hypothesis specifically within this population. Second, we used cfPWV, which is considered the gold standard for assessing arterial stiffness. Third, we adjusted for mean blood pressure derived from 24-h blood pressure monitoring. Fourth, our analysis involved comprehensive adjustments for a wide range of potential confounding variables, and our results were robust after many additional adjustments.\n\nThe present study has some limitations. First, due to the cross-sectional design, we cannot draw conclusions about causality. Reverse causality is also possible, as previous research suggests that diabetic neuropathy may contribute to arterial stiffening through mechanisms, such as reduced vascular innervation and increased arterial calcification [ 38 ]. Second, residual confounding cannot be excluded. We did not account for potential shared pathophysiological mechanisms such as endothelial dysfunction, low-grade inflammation, and oxidative stress, which may underlie both neuropathy [ 39 ] and arterial stiffness [ 40 ], which may have overestimated our results. Third, our study primarily focused on a Caucasian population aged 40–75 years. Consequently, the generalizability of our findings to other demographic groups and age ranges remains uncertain. Further research is required to investigate these associations in diverse ethnic populations and across different age groups.\n\nIn conclusion, the present population-based study demonstrated that greater arterial stiffness, determined by cfPWV, was associated with ocular (small) and peripheral (large) fiber neuropathy. These results were independent of important confounders, such as diabetes, hypertension, renal insufficiency, and prior cardiovascular disease. Future longitudinal research is needed to clarify whether arterial stiffening is a direct cause of neuropathy.\n\n— Source (discussion, peer-reviewed): Chidera Okoro, Carla J.H. van der Kallen, Sara B.A. Mokhtar, et al. · (2025) · \"Arterial stiffness is associated with small and large fiber neuropathy: The Maastricht Study\" · Journal of Hypertension · doi: 10.1097/HJH.0000000000004126 · PMCID: PMC12582623 · PMID: 41123059\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12174315-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12174315", "pmid": "40527903", "doi": "10.1038/s41467-025-60813-2", "title": "Stable heritability of type 1 diabetes in a Swedish Nationwide Cohort Study", "journal": "Nature Communications", "publication_year": 2025, "citation": "Yuxia Wei, Tomas Andersson, Shengxin Liu, et al. · (2025) · \"Stable heritability of type 1 diabetes in a Swedish Nationwide Cohort Study\" · Nature Communications · doi: 10.1038/s41467-025-60813-2 · PMCID: PMC12174315 · PMID: 40527903", "question": "What is the published background on \"Stable heritability of type 1 diabetes in a Swedish Nationwide Cohort Study\"? Cite a peer-reviewed source.", "answer": "The incidence of childhood-onset type 1 diabetes (T1D) has been increasing worldwide since the 1950s, with an annual increase of 3–4% 1 , 2 . It is unclear if this trend is due to a rise in nongenetic (environmental) risk factors, increasing genetic susceptibility of the population or a combination.\n\nEnvironmental explanations are generally favored since it seems unlikely that the genetic makeup of the population changes in a few decades and because incidence varies markedly between genetically similar populations 1 , 3 . Notably, the rise in T1D coincides with a rise in childhood obesity 4 , a proposed risk factor for T1D 5 , 6 . Other suggested risk factors include early-life factors like maternal smoking (protective) 7 , higher maternal age at delivery 8 and breastfeeding (protective) 9 . To what extent the prevalence of these factors has changed and contributed to a rise in the incidence of T1D is unclear.\n\nHeritability is the proportion of phenotypic variance (including variance explained by genetic and environmental factors) in a disease explained by all genetic factors. T1D heritability has been estimated at between 50% and 88% in twin or other family-based studies of different populations 10 – 13 and we recently estimated it at 81% in Swedish children 14 . If the increasing T1D incidence is mainly driven by environmental factors, the relative contribution of environmental factors to T1D variance would be expected to increase and heritability decrease over time 15 . As far as we know, no previous study has investigated whether T1D heritability has changed over the last decades. However, a previous study from Australia indicates that the proportion of T1D cases with the highest-risk human leukocyte antigen (HLA) genotypes has decreased while the proportion of affected children with intermediate-risk HLA genotypes increased from 1980s to 2000s 16 . Similar findings have been reported from Finland, Sweden, US, and the UK when comparing cases diagnosed 1985-2008 to those diagnosed earlier 17 – 20 . This indicates that the contribution of HLA genotypes to T1D risk has changed but not lessened over time 16 . Still, only approximately half of the genetic risks of T1D is accounted for by HLA genotypes 16 and a rise in genetic susceptibility could be driven by risk alleles outside of the HLA complex. T1D proposedly has age-related endotypes, with distinct etiology and pathogenesis between individuals diagnosed before the age of seven and those diagnosed after the age of thirteen 21 . The genetic contribution to the etiology of these endotypes is scarcely investigated.\n\nIn this work, we set out to clarify if the environmental and genetic influences on childhood-onset T1D (0–18 years) have changed in Sweden over the last 30 years. We analyze the trend of T1D incidence and heritability among three million children born from 1982 to 2010 using nationwide data. We show that the heritability of T1D and its endotypes has remained stable over time. We identify environmental factors associated with T1D and find that changing prevalence of them could only explain a small proportion of the increasing T1D incidence, indicating that they are not the major driver of the rise in T1D.\n\n— Source (introduction, peer-reviewed): Yuxia Wei, Tomas Andersson, Shengxin Liu, et al. · (2025) · \"Stable heritability of type 1 diabetes in a Swedish Nationwide Cohort Study\" · Nature Communications · doi: 10.1038/s41467-025-60813-2 · PMCID: PMC12174315 · PMID: 40527903\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12888146-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC12888146", "pmid": "41526884", "doi": "10.1186/s12913-025-13676-8", "title": "Facilitating a complex behaviour-change intervention: healthcare professionals’ accounts of their journeys to competence and confidence", "journal": "BMC Health Services Research", "publication_year": 2026, "citation": "Ruth I. Hart, Christina Sheehan, Debbie Brewin, et al. · (2026) · \"Facilitating a complex behaviour-change intervention: healthcare professionals’ accounts of their journeys to competence and confidence\" · BMC Health Services Research · doi: 10.1186/s12913-025-13676-8 · PMCID: PMC12888146 · PMID: 41526884", "question": "What is the published background on \"Facilitating a complex behaviour-change intervention: healthcare professionals’ accounts of their journeys to competence and confidence\"? Cite a peer-reviewed source.", "answer": "High-quality health-related information has been described as ‘the lifeblood of good health and wellbeing … allow(ing) us to understand how to improve our own and our family’s health’[ 1 (p.7)]. Access to such information is now firmly embedded in UK health policy [ 1 , 2 ] and its provision is a key component of many healthcare professionals’ work. However, it has become increasingly clear that where behaviour change is the goal, information may be necessary, yet not sufficient [ 3 , 4 ]. To bring about and/or sustain behaviour change, other approaches, techniques and tools, informed by behavioural theory and science may be needed [ 2 , 4 – 7 ]. Hence, in recent years, healthcare professionals have been tasked not only with information provision, but also with delivering brief, evidence-based, behaviour-change interventions, as an adjunct to routine practice [ 4 , 8 ]. In addition, in the absence of sufficient specialists with expertise in the fields of psychology and/or behaviour change, interest has been growing in whether healthcare professionals from other, disparate backgrounds can facilitate the delivery of more extended and ‘complex’ behaviour-change interventions [ 9 – 12 ]. Such interventions target individuals with complicated health needs (e.g., arising from a chronic condition), have multiple components, and incorporate more sophisticated behaviour-change techniques. They are typically delivered over a number of relatively lengthy (e.g., 30 minutes-plus) sessions.\n\nA small but growing body of research has examined different healthcare professionals’ experiences of, and perspectives on, this emerging area of work. The research provides qualified support for the involvement of non-specialists in the delivery of complex behaviour-change interventions, and some useful insights. For instance, a recent systematic review of 17 research studies investigating the motivational interviewing skills of healthcare professionals working in diabetes care concluded that, subsequent to training, some such professionals employed some relevant techniques [ 13 ]. However, as Kaczmarek et al. further observed, the techniques those professionals employed tended to be ones which were less challenging to learn and apply, e.g., increased use of open questions and ‘change statements’ (i.e., articulations of the rationale, or motivation for, change) [ 13 ]. Jongebloed-Westra et al. similarly concluded that healthcare professionals (specifically podiatrists) could be trained to use basic motivational interviewing techniques successfully in interactions with patients [ 14 ]. In terms of the factors supportive of healthcare professionals developing and employing more complex skills in facilitating behaviour change, several studies have highlighted the importance of adequate preparatory training, and/or ongoing, ‘in-service’ training, supervision, and support [ 13 , 15 – 19 ]. These findings are valuable, but understanding of the circumstances in which healthcare professionals from different disciplinary backgrounds become competent and confident facilitators of behaviour change remains far from complete.\n\nThus, as part of a wider evaluation of a novel, person-centred, cognitive behavioural intervention, designed to bring about changes in the self-care behaviours of individuals with a history of diabetes and foot ulceration, we set out to examine facilitators’ development more closely. This complex intervention, ‘REDUCE,’ (see Box 1 for more details) was facilitated by a team of registered and accredited healthcare professionals from a range of disciplines (nursing, podiatry, and psychology/talking therapies). Healthcare professionals were employed specifically to deliver the intervention by the study sponsor (University Hospitals of Derby and Burton NHS Foundation Trust). Further information on the facilitator recruitment process and their employment arrangements is provided in the Methods (Participants and recruitment) section, below.\n\nAll healthcare professionals appointed as REDUCE facilitators were required to complete intervention-specific training before being assigned any intervention participants. That training covered the therapeutic approach, use of specific behaviour-change techniques, and, for the benefit of those without relevant expertise, diabetes and diabetic foot health. We describe the organisation and content of the REDUCE facilitator training, and how it evolved over time, in detail elsewhere [ 20 ]. In brief, all facilitator training was provided virtually (i.e., on-line) over several days, to small groups of healthcare professionals. It involved a mixture of didactic and interactive components, and was designed and delivered by three experienced Cognitive Behavioural Therapy (CBT) therapists, with contributions from research team members. Trainee facilitators were also expected to undertake some homework/self-study between sessions, such as reading the participant and facilitator handbooks. Following training and alongside delivery of the intervention, facilitators were offered regular one-to-one clinical supervision and/or group-based support, with or facilitated by an experienced and accredited CBT supervisor, based at a collaborating UK university.\n\nIn this report, we consider whether, how, and why, the healthcare professionals appointed and trained as REDUCE facilitators perceived themselves as having developed competence and confidence in performing their facilitator role. In particular, we explore the influence and impact of training, supervision, and other, previously unrecognised factors (e.g., independent learning) on facilitators’ development. In so doing, our aim was to generate insights that might support the judicious recruitment, training, development, and retention of appropriately skilled facilitators to REDUCE and/or other, similar behaviour change-oriented programmes in the future.\n\nBox 1 Outline of the intervention REDUCE : • Is a complex behaviour-change intervention designed for people (≥ 18 years) with diabetes who have recently had a diabetic foot ulcer (DFU) but on enrolment are ulcer-free. • Aims to increase the time people spend ulcer-free, by avoiding or delaying reoccurrence of a DFU, and decreasing time to healing if/when a new DFU develops. • Seeks to establish a suite of behaviours supportive of the above aims, including: effective daily foot-checking; rapid help-seeking (where changes are identified); regular and graded (i.e., appropriate) physical activity; and, personalised strategies for managing low mood. • Uses an approach informed by Cognitive Behavioural Therapy (CBT), specifically the idea that thoughts, feelings, and actions/behaviours are linked. Modifying thoughts/beliefs may therefore be necessary to change behaviours, and changing thoughts/beliefs or behaviours may change feelings. Facilitators work with participants to identify problems (e.g., barriers to behavioural change) and break these down into separate, smaller and more manageable parts for resolution. • Employs a range of recognised behaviour-change techniques including: information provision; goal setting; action-planning; self-monitoring; habit formation; use of prompts; positive re-framing; behavioural experiments; and, behavioural activation. • Is delivered remotely (by telephone or video-call) to participants around England over eight 60-minute sessions. It is supplemented by paper and digital resources available to participants during and beyond those eight sessions.\n\nOur interviewees revealed diverse and interesting backgrounds, with the sample including individuals who said they were still working, or had until recently worked, in podiatry, nursing, and/or psychology/talking therapies. Some reported having worked in more than one of these disciplines – for example, starting out as a nurse and then re-training as a podiatrist. A few also had experience in higher education, including delivering pre-registration training. Several were partially retired, and working reduced or part-time hours in one or more other roles.\n\nWhen asked how they became aware of the REDUCE programme, interviewees recalled a variety of channels. Two had been involved for many years, and delivered an earlier (group-based) version of the intervention. Others explained how they were known to and had been approached by another professional involved with REDUCE (e.g., a research team member and/or a clinical colleague), who, they surmised, perceived them as having the relevant skills and capacity to contribute: (Investigator) used to be the consultant in our foot clinic … she knew I’d reduced my hours , so she approached me (about REDUCE). (Cath).\n\nSeveral described having seen targeted advertising disseminated through relevant professional bodies (e.g., the Royal Colleges) and/or more informal professional networks (see Supplementary File).\n\nThese healthcare professionals offered varied, and often multifactorial, motives for applying to be a REDUCE facilitator. The character of the intervention was often cited as a draw, with interviewees highlighting its alignment with longstanding, personal interests in health behaviour and/or psychology (see Supplementary File). Several contrasted the REDUCE model with the more medically-oriented approaches underpinning their routine work and/or indicated frustration with the constraints of practice in the NHS. Such interviewees said they had seized the opportunity to work in more satisfying ways: The reason for doing this was … I found when I worked in diabetes , is , it’s very much a medical model , and I got very frustrated with it. And then I got very excited by hearing this. So that’s why I wanted to be involved. (Josie).\n\nOther interviewees said they were motivated by the prospect of extending their knowledge and/or skills (of preventive footcare or, more commonly, psychological therapies) either to enhance their current practice or to accrue experience supportive of longer-term career ambitions: I saw this role , and I thought , this is brilliant … (because) my kind of goal was to also become a CBT therapist , which I’ve now trained as! (Regina).\n\nPragmatic factors were also cited by some. For those based in less populous regions, where possibilities for exploring new roles were more limited, remote working was portrayed as offering a welcome, logistically straightforward, development opportunity. A few others noted how they were attracted by REDUCE’s flexible employment arrangements and the rare opportunity (for those employed within the NHS) to work from home: (Husband)’s totally retired … (and) I’m 58 , so I’m slowing down , I’m moving to retirement at 60 , and I wanted to just work at home. (Frederica).\n\n— Source (introduction, peer-reviewed): Ruth I. Hart, Christina Sheehan, Debbie Brewin, et al. · (2026) · \"Facilitating a complex behaviour-change intervention: healthcare professionals’ accounts of their journeys to competence and confidence\" · BMC Health Services Research · doi: 10.1186/s12913-025-13676-8 · PMCID: PMC12888146 · PMID: 41526884\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-10364866-intro", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-intro", "source": "PubMed Central open-access full text", "pmcid": "PMC10364866", "pmid": "34270711", "doi": "10.1093/bjs/znab199", "title": "Adrenalectomy for incidental and symptomatic phaeochromocytoma: retrospective multicentre study based on the Eurocrine® database", "journal": "The British Journal of Surgery", "publication_year": 2021, "citation": "L Hallin Thompson, Ö Makay, L Brunaud, et al. · (2021) · \"Adrenalectomy for incidental and symptomatic phaeochromocytoma: retrospective multicentre study based on the Eurocrine® database\" · The British Journal of Surgery · doi: 10.1093/bjs/znab199 · PMCID: PMC10364866 · PMID: 34270711", "question": "What is the published background on \"Adrenalectomy for incidental and symptomatic phaeochromocytoma: retrospective multicentre study based on the Eurocrine® database\"? Cite a peer-reviewed source.", "answer": "Phaeochromocytoma is a neuroendocrine, catecholamine-secreting tumour, arising from chromaffin cells of the adrenal medulla. Clinical presentation is variable, and depends on the magnitude, type, and pattern of hormone release (adrenaline, noradrenaline, and dopamine), as well as individual sensitivity to catecholamines and their metabolites 1 , 2 .\n\nClinical presentation includes a triad of symptoms: headache, sweating, and palpitations 1 . Other symptoms include anxiety, tremor, nausea, dyspnoea, and abdominal pain. Hypertension is a common sign of phaeochromocytoma, reported in up to 78–93 per cent of patients with adrenal and extra-adrenal phaeochromocytoma 3 , 4 . Only 0.04 per cent of patients with hypertension are, however, diagnosed with a phaeochromocytoma 5 . Paroxysmal catecholamine release may cause sudden peaks in BP, leading to severe cardiovascular events. Preoperative α-adrenergic blockade is recommended by guidelines to prevent vasoconstriction, and perioperative cardiovascular complications and death 6 . With improvements in anaesthetic methods and minimally invasive surgery, this practice has recently come under scrutiny. A meta-analysis by Schimmack and colleagues 7 demonstrated a lack of evidence for preoperative α-blockade. Most larger series of patients who had surgery for phaeochromocytoma have, however, been reported from high-volume tertiary centres and the results might therefore suffer from selection bias 8 , 9 .\n\nAn increasing proportion of phaeochromocytomas are discovered as adrenal incidentalomas. Phaeochromocytomas without clinical symptoms represent 4–7 per cent of adrenal incidentalomas 10–12 . Among histologically diagnosed phaeochromocytomas, up to 29 per cent were detected as incidentalomas 3 .\n\nThe aim of this study was to investigate contemporary clinical features, evaluation, preoperative medical treatment, surgery, and outcome in patients undergoing adrenalectomy for phaeochromocytoma. A special focus was to analyse outcomes for those diagnosed by clinical symptoms compared with incidentalomas, and in patients with or without preoperative treatment with α-blockers. Data were retrieved from Eurocrine®, a pan-European quality registry for endocrine tumours.\n\n— Source (introduction, peer-reviewed): L Hallin Thompson, Ö Makay, L Brunaud, et al. · (2021) · \"Adrenalectomy for incidental and symptomatic phaeochromocytoma: retrospective multicentre study based on the Eurocrine® database\" · The British Journal of Surgery · doi: 10.1093/bjs/znab199 · PMCID: PMC10364866 · PMID: 34270711\nLicense: CC-BY-NC. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12711119-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC12711119", "pmid": "41417370", "doi": "10.1590/1806-9282.20251162", "title": "Misoprostol combined with artificial membrane stripping showed the best effect of induction among women with gestational diabetes mellitus: a retrospective cohort study", "journal": "Revista da Associação Médica Brasileira", "publication_year": 2025, "citation": "Xuemei Li, Qimei Yang, Xia Zhang, et al. · (2025) · \"Misoprostol combined with artificial membrane stripping showed the best effect of induction among women with gestational diabetes mellitus: a retrospective cohort study\" · Revista da Associação Médica Brasileira · doi: 10.1590/1806-9282.20251162 · PMCID: PMC12711119 · PMID: 41417370", "question": "Summarize the abstract of the paper titled \"Misoprostol combined with artificial membrane stripping showed the best effect of induction among women with gestational diabetes mellitus: a retrospective cohort study\".", "answer": "The aim of this study was to explore the optimal method of induction of labor in women with gestational diabetes mellitus and its impact on delivery outcomes.\n\nThis retrospective cohort study was conducted among nulliparous women with gestational diabetes mellitus delivering at the First Affiliated Hospital of Fujian Medical University and the First People's Hospital of Yunnan Province from 2018 to 2023. Data were extracted from electronic medical records.\n\nA total of 600 patients who delivered met the inclusion criteria: the double-balloon group (Group B, n=198), the misoprostol vaginal insert group (Group M, n=200), and the Misoprostol combined with artificial membrane stripping group (Group MA, n=202). Group MA showed higher induction of labor success rates (93.5%) compared to Group M (86.0%) and Group B (81.5%, p=0.002). The time to labor onset was shortest in Group MA (32.5±6.5 h), followed by Group M (35.8±2.5 h) and Group B (45.8±4.5 h, p<0.001). Vaginal delivery time was also significantly shorter in Group MA (47.4±4.3 h) compared to Group M (49.1±7.4 h) and Group B (57.1±5.7 h, p<0.001). Chorioamnionitis rates were lower in Group MA (2.5%) and Group M (3.0%) compared to Group B (8.5%, p=0.007). No significant differences were observed between groups for cesarean rates, fetal distress, abnormal labor, or neonatal outcomes (p>0.05).\n\nThe combination of misoprostol vaginal insert and artificial membrane stripping effectively enhances cervical ripening and improves vaginal delivery success in gestational diabetes mellitus patients, providing a promising strategy for labor induction.\n\n— Source (abstract, peer-reviewed): Xuemei Li, Qimei Yang, Xia Zhang, et al. · (2025) · \"Misoprostol combined with artificial membrane stripping showed the best effect of induction among women with gestational diabetes mellitus: a retrospective cohort study\" · Revista da Associação Médica Brasileira · doi: 10.1590/1806-9282.20251162 · PMCID: PMC12711119 · PMID: 41417370\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-7617696-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC7617696", "pmid": "39146468", "doi": "10.1089/dia.2024.0298", "title": "Safety of options to ″Boost″ (enhancing insulin infusion rates) and ″Ease-off″ (reducing insulin infusion rates) in CamAPS FX Hybrid Closed-Loop system: a real-world analysis", "journal": "Diabetes technology & therapeutics", "publication_year": 2024, "citation": "Chloë Royston, Simon Bergford, Peter Calhoun, et al. · (2024) · \"Safety of options to ″Boost″ (enhancing insulin infusion rates) and ″Ease-off″ (reducing insulin infusion rates) in CamAPS FX Hybrid Closed-Loop system: a real-world analysis\" · Diabetes technology & therapeutics · doi: 10.1089/dia.2024.0298 · PMCID: PMC7617696 · PMID: 39146468", "question": "Summarize the abstract of the paper titled \"Safety of options to ″Boost″ (enhancing insulin infusion rates) and ″Ease-off″ (reducing insulin infusion rates) in CamAPS FX Hybrid Closed-Loop system: a real-world analysis\".", "answer": "The usage and safety of the Boost and Ease-off features in the CamAPS FX hybrid closed-loop system was analysed in a retrospective analysis of real-world data from 7,464 users over a 12-month period. Boost was used more frequently than Ease-off, but for a shorter duration per use. Mean starting glucose was above range for Boost (229±51 mg/dL), and within range for Ease-off (114±29 mg/dL). Time spent below 70 mg/dL was low during Boost periods [median (IQR) 0.0% (0.0, 0.5%)], and lower than during no Boost periods [2.1% (1.2, 3.4%)], while time spent above 180 mg/dL was lower during Ease-off periods (15±14%) compared to no Ease-off periods (25±12%). There were no episodes of severe hypoglycaemia or DKA attributed to Boost or Ease-off use. Boost and Ease-off allow users to engage safely with CamAPS FX to manage their glucose levels during periods of more-than-usual and less-than-usual insulin needs.\n\n— Source (abstract, peer-reviewed): Chloë Royston, Simon Bergford, Peter Calhoun, et al. · (2024) · \"Safety of options to ″Boost″ (enhancing insulin infusion rates) and ″Ease-off″ (reducing insulin infusion rates) in CamAPS FX Hybrid Closed-Loop system: a real-world analysis\" · Diabetes technology & therapeutics · doi: 10.1089/dia.2024.0298 · PMCID: PMC7617696 · PMID: 39146468\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}
{"id": "pmc-12705128-abstract", "specialty": "diabetic-companion", "domain": "diabetes", "tier": "royal-jelly", "bucket": "pmc-full-text-abstract", "source": "PubMed Central open-access full text", "pmcid": "PMC12705128", "pmid": "41397294", "doi": "10.2196/75672", "title": "Low-Carbohydrate Nutrition Counseling With Continuous Glucose Monitoring to Improve Metabolic Health Among Veterans With Type 2 Diabetes: Pilot Quality Improvement Initiative Study", "journal": "JMIR Diabetes", "publication_year": 2025, "citation": "Cassie D Turner, Kishor Patel, Katherine Freeman, et al. · (2025) · \"Low-Carbohydrate Nutrition Counseling With Continuous Glucose Monitoring to Improve Metabolic Health Among Veterans With Type 2 Diabetes: Pilot Quality Improvement Initiative Study\" · JMIR Diabetes · doi: 10.2196/75672 · PMCID: PMC12705128 · PMID: 41397294", "question": "Summarize the abstract of the paper titled \"Low-Carbohydrate Nutrition Counseling With Continuous Glucose Monitoring to Improve Metabolic Health Among Veterans With Type 2 Diabetes: Pilot Quality Improvement Initiative Study\".", "answer": "One in 4 Veterans who receive care through the Veterans Health Administration has type 2 diabetes (T2D). Dietary carbohydrate restriction can promote weight loss and improve blood glucose control, but Veterans taking certain medications (eg, insulin) may experience serious complications (eg, hypoglycemia) without adequate support and monitoring.\n\nThis study aims to develop and evaluate the feasibility, acceptability, and clinical effectiveness of a pilot low-carbohydrate (LC) nutrition counseling program guided by continuous glucose monitoring (CGM) for Veterans with T2D receiving insulin (ie, LC-CGM).\n\nThis is a pragmatic, nonrandomized, pre-post quality improvement pilot program. Eligible patients were Veterans with T2D who were prescribed ≥3 daily injections of insulin. The 24-week LC-CGM program consisted of virtual visits with a registered dietitian (RD) and clinical pharmacy practitioner (CPP); CGM data were used to guide tailored nutrition counseling and de-escalation or cessation of glucose-lowering medications. To evaluate changes from baseline, intention-to-treat analyses were conducted for all enrollees, with separate analyses for program completers. Primary outcomes were program feasibility and acceptability (ie, program enrollment and completion rates and mean number of RD and CPP visits). Secondary outcomes included mean weight change, percent weight loss, achievement of ≥5% and ≥10% weight loss, change in glucose-lowering medication use, and change in laboratory measures (eg, hemoglobin A 1c [HbA 1c ]).\n\nProgram evaluation occurred from March 19, 2021, to May 3, 2024. Among 43 Veterans referred to the LC-CGM program, 38 (88%) enrolled. Most were men (37/38, 97%), white (29/38, 76%), with an average age of 63.7 (SD 9.6) years. Mean BMI and HbA 1c were 38.1 (SD 5.8) kg/m 2 and 7.8% (SD 1.3). Of 38 enrollees, 27 (71%) completed the program. Enrollees averaged 9.5 (SD 3.3) RD visits and 12.8 (SD 4.7) CPP visits. In intention-to-treat analyses, mean weight change was −11.5 kilograms (SD 8.7; 95% CI −14.4 to −8.6), corresponding to 9.5% weight loss (SD 7.2; 95% CI −14.9 to −4.2), with 58% (22/38) achieving ≥5% weight loss and 32% (12/38) achieving ≥10% weight loss. Overall, use of glucose-lowering medications decreased from 3.5 (SD 0.8) per patient at baseline to 2.4 (SD 0.9) per patient at 24 weeks ( P <.001), with 72% (26/36) of Veterans discontinuing short-acting insulin and 50% (18/36; P <.001) discontinuing long-acting insulin. Use of glucagon-like peptide-1 receptor agonists increased from 39% (15/38) at baseline to 61% (23/38) at 24 weeks ( P =.02). Among program completers (n=27), mean percent weight loss was −11.8% (SD 6.5) and median HbA 1c decreased by 0.7% (95% CI −0.9 to −0.3; P =.001).\n\nThis pilot program provides preliminary evidence that supports feasibility, acceptability, and clinical effectiveness among Veterans with T2D. Additional research is needed to rigorously test longer-term clinical and cost-effectiveness among a larger cohort of eligible Veterans.\n\n— Source (abstract, peer-reviewed): Cassie D Turner, Kishor Patel, Katherine Freeman, et al. · (2025) · \"Low-Carbohydrate Nutrition Counseling With Continuous Glucose Monitoring to Improve Metabolic Health Among Veterans With Type 2 Diabetes: Pilot Quality Improvement Initiative Study\" · JMIR Diabetes · doi: 10.2196/75672 · PMCID: PMC12705128 · PMID: 41397294\nLicense: CC-BY. Retrieved from PubMed Central full text.\n\nNote: This reproduces published research findings. It is not individualized medical advice. Please discuss your situation with your healthcare provider or care team."}