Pub Date : 2026-03-01Epub Date: 2026-03-05DOI: 10.1016/j.diabet.2026.101746
Cathy J. Sun , Valérie Savard , Cindye Audet , Rémi Rabasa-Lhoret
Amidst the worldwide physician shortage, we share how realizing our vision can improve access to diabetes care. Central to this vision is a methodical process to assess each patient’s complexity in order to delegate their care within a medically-supervised interdisciplinary comprehensive care clinic.
{"title":"Realizing a vision to improve access to diabetes care","authors":"Cathy J. Sun , Valérie Savard , Cindye Audet , Rémi Rabasa-Lhoret","doi":"10.1016/j.diabet.2026.101746","DOIUrl":"10.1016/j.diabet.2026.101746","url":null,"abstract":"<div><div>Amidst the worldwide physician shortage, we share how realizing our vision can improve access to diabetes care. Central to this vision is a methodical process to assess each patient’s complexity in order to delegate their care within a medically-supervised interdisciplinary comprehensive care clinic.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101746"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147373644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Toe necrosis is a common complication of diabetic foot ulcer (DFU). Amputation surgery is usually performed by a surgeon in the operating room. In response to the limited availability of operating rooms, clinicians from two specialized diabetic foot units performed bedside surgery to amputate isolated toe-necrosis-complicated DFU.
The aim of our study was to compare the rate of wound healing 6 months after toe amputation following bedside amputation surgery (BAS) and conventional amputation surgery (CAS).
Methods
This retrospective observational multi-center study was conducted in two French diabetic foot units. All patients with diabetes mellitus (DM) who underwent a toe amputation for isolated necrosis in an operating room (CAS) or at bedside (BAS) were included (05/2016 – 07/2023). The primary endpoint was the 6-month healing rate, defined as a complete skin epithelialization without recurrence at 6 months, without secondary amputation.
Results
Out of 2029 patients admitted for DFU, 189 had isolated toe necrosis requiring limited amputation (9%). Among the 171 patients who attended follow-up at 6 months: males 82.5%, type 2 DM 94.7%, average duration of DM 18.3 ± 0.9years, average HbA1c 8.6 ± 2%. BAS was performed on 106/171(62%) patients. The 6-month healing rate was not significantly different between the two groups (BAS 53.8% vs CAS 52.3%, P = 0.852). The rate of secondary surgery was not significantly different (BAS 24.5% vs CAS 16.9%, P = 0.241).
Conclusion
BAS is a safe and efficient approach for the treatment of isolated toe necrosis, resulting in a healing rate similar to that of conventional surgery.
目的：脚趾坏死是糖尿病足溃疡（DFU）的常见并发症。截肢手术通常由外科医生在手术室进行。由于手术室的可用性有限，来自两个专门的糖尿病足科室的临床医生进行了床边手术，切除了孤立的脚趾坏死合并的DFU。我们的研究目的是比较床边截肢手术（BAS）和常规截肢手术（CAS）后6个月脚趾截肢的伤口愈合率。方法：这项回顾性观察性多中心研究在两个法国糖尿病足单位进行。所有因孤立性坏死在手术室（CAS）或床边（BAS）接受脚趾截肢的糖尿病（DM）患者被纳入研究（2016年5月- 2023年7月）。主要终点是6个月的愈合率，定义为6个月完全皮肤上皮化，无复发，无继发截肢。结果：在入院的2029例DFU患者中，189例有孤立性脚趾坏死，需要有限截肢（9%）。随访6个月的171例患者中：男性82.5%，2型糖尿病94.7%，糖尿病平均病程18.3±0.9年，平均HbA1c 8.6±2%。171例患者中有106例（62%）接受了BAS。两组6个月的治愈率差异无统计学意义（BAS 53.8% vs CAS 52.3%, P = 0.852）。两组患者的二次手术率差异无统计学意义（BAS 24.5% vs CAS 16.9%, P = 0.241）。结论：BAS是一种安全有效的治疗孤立性足趾坏死的方法，其治愈率与常规手术相似。
{"title":"Bedside amputation surgery for isolated toe necrosis in diabetes units as an alternative to conventional amputation in surgery units","authors":"Florine Féron , Jean-Philippe Kevorkian , Jean-Baptiste Julla , Nadjet Ghozlane , Serge Aho Glele , Coralie Fourmont , Jean-Michel Petit , Jean-François Gautier , Mathilde Didier , Benjamin Bouillet","doi":"10.1016/j.diabet.2026.101727","DOIUrl":"10.1016/j.diabet.2026.101727","url":null,"abstract":"<div><h3>Aim</h3><div>Toe necrosis is a common complication of diabetic foot ulcer (DFU). Amputation surgery is usually performed by a surgeon in the operating room. In response to the limited availability of operating rooms, clinicians from two specialized diabetic foot units performed bedside surgery to amputate isolated toe-necrosis-complicated DFU.</div><div>The aim of our study was to compare the rate of wound healing 6 months after toe amputation following bedside amputation surgery (BAS) and conventional amputation surgery (CAS).</div></div><div><h3>Methods</h3><div>This retrospective observational multi-center study was conducted in two French diabetic foot units. All patients with diabetes mellitus (DM) who underwent a toe amputation for isolated necrosis in an operating room (CAS) or at bedside (BAS) were included (05/2016 – 07/2023). The primary endpoint was the 6-month healing rate, defined as a complete skin epithelialization without recurrence at 6 months, without secondary amputation.</div></div><div><h3>Results</h3><div>Out of 2029 patients admitted for DFU, 189 had isolated toe necrosis requiring limited amputation (9%). Among the 171 patients who attended follow-up at 6 months: males 82.5%, type 2 DM 94.7%, average duration of DM 18.3 ± 0.9years, average HbA1c 8.6 ± 2%. BAS was performed on 106/171(62%) patients. The 6-month healing rate was not significantly different between the two groups (BAS 53.8% vs CAS 52.3%, <em>P</em> = 0.852). The rate of secondary surgery was not significantly different (BAS 24.5% vs CAS 16.9%, <em>P</em> = 0.241).</div></div><div><h3>Conclusion</h3><div>BAS is a safe and efficient approach for the treatment of isolated toe necrosis, resulting in a healing rate similar to that of conventional surgery.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101727"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146004910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-12DOI: 10.1016/j.diabet.2026.101726
Jessica L Harding , Tegveer S Uppal , Dunya Tomic , Mohammed K Ali , Agus Salim , Dianna J Magliano
Objective
The true burden of diabetes is likely underestimated by not considering the full range of complications associated with diabetes. Our aim was to compare cause-specific hospitalizations in adults with vs. without diabetes.
Research Design and Methods
Our denominator included all adults with and without self-reported diabetes from the 2019 Behavioral Risk Factor Surveillance System Survey, weighted to reflect the U.S. population. Our numerator, age-standardized risks of ICD-10-CM-defined inpatient hospitalizations and emergency department (ED) visits, were identified from the 2019 National Inpatient Sample and National ED Sample, respectively, weighted to be representative of U.S. hospitalizations. Each cause-specific hospitalization was classified as traditional, emerging, or other.
Results
For inpatient hospitalizations, the highest absolute risk difference per classification was for sepsis (traditional; 1,680 [95%CI: 1,649–1,712] hospitalizations per 100,000), pneumonia (emerging; 225 [218–232]), and respiratory failure (other; 280 [272–289]). For ED visits, the highest absolute risk difference was for abscess, furuncle, and carbuncle (traditional; 388 [352–423] visits per 100,000), complications of cardiac devices (emerging; 111 [104–118]), and disorders of the urinary system (other; 299 [252–346]).
Conclusions
The causes of excess hospitalizations associated with diabetes extend well beyond traditional complications with implications for population-level planning, resource allocation, and individual diabetes management.
{"title":"Excess burden of hospitalizations in adults with diabetes – a national US cross-sectional study","authors":"Jessica L Harding , Tegveer S Uppal , Dunya Tomic , Mohammed K Ali , Agus Salim , Dianna J Magliano","doi":"10.1016/j.diabet.2026.101726","DOIUrl":"10.1016/j.diabet.2026.101726","url":null,"abstract":"<div><h3>Objective</h3><div>The true burden of diabetes is likely underestimated by not considering the full range of complications associated with diabetes. Our aim was to compare cause-specific hospitalizations in adults with vs. without diabetes.</div></div><div><h3>Research Design and Methods</h3><div>Our denominator included all adults with and without self-reported diabetes from the 2019 Behavioral Risk Factor Surveillance System Survey, weighted to reflect the U.S. population. Our numerator, age-standardized risks of ICD-10-CM-defined inpatient hospitalizations and emergency department (ED) visits, were identified from the 2019 National Inpatient Sample and National ED Sample, respectively, weighted to be representative of U.S. hospitalizations. Each cause-specific hospitalization was classified as traditional, emerging, or other.</div></div><div><h3>Results</h3><div>For inpatient hospitalizations, the highest absolute risk difference per classification was for sepsis (traditional; 1,680 [95%CI: 1,649–1,712] hospitalizations per 100,000), pneumonia (emerging; 225 [218–232]), and respiratory failure (other; 280 [272–289]). For ED visits, the highest absolute risk difference was for abscess, furuncle, and carbuncle (traditional; 388 [352–423] visits per 100,000), complications of cardiac devices (emerging; 111 [104–118]), and disorders of the urinary system (other; 299 [252–346]).</div></div><div><h3>Conclusions</h3><div>The causes of excess hospitalizations associated with diabetes extend well beyond traditional complications with implications for population-level planning, resource allocation, and individual diabetes management.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101726"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-24DOI: 10.1016/j.diabet.2026.101743
Theocharis Koufakis , Vasileios Tsimihodimos , Djordje S. Popovic
Research on the developmental origins of health and disease has traditionally centered on maternal health and in utero exposures, with comparatively limited attention to paternal preconception factors. However, emerging evidence suggests that paternal metabolic health—particularly obesity and diabetes—may contribute to offspring metabolic risk. Observational studies associate higher paternal body mass index and cardiometabolic dysfunction with increased offspring adiposity, blood pressure, and markers of insulin resistance, although effect sizes are modest and confounding by shared genetics and environment remains a key limitation. Mechanistic data from animal models support sperm-mediated epigenetic pathways linking paternal metabolic status to offspring metabolic programming, yet human epigenetic evidence is inconsistent. At the same time, the widespread use of modern obesity pharmacotherapies, including glucagon-like peptide-1 receptor agonists and dual incretin agonists, has introduced a largely unexamined dimension of paternal exposure. Current data on paternal use of these agents and long-term offspring metabolic outcomes are sparse and fragmentary. As obesity pharmacotherapy expands among men of reproductive age, a shift beyond maternal-only frameworks is warranted. Rigorous studies integrating paternal metabolic profiling, medication exposure, and long-term offspring follow-up are urgently needed to inform clinical practice and public health guidance.
{"title":"Half the genome, half the story? Paternal metabolic health and offspring outcomes in the era of modern obesity pharmacotherapy","authors":"Theocharis Koufakis , Vasileios Tsimihodimos , Djordje S. Popovic","doi":"10.1016/j.diabet.2026.101743","DOIUrl":"10.1016/j.diabet.2026.101743","url":null,"abstract":"<div><div>Research on the developmental origins of health and disease has traditionally centered on maternal health and in utero exposures, with comparatively limited attention to paternal preconception factors. However, emerging evidence suggests that paternal metabolic health—particularly obesity and diabetes—may contribute to offspring metabolic risk. Observational studies associate higher paternal body mass index and cardiometabolic dysfunction with increased offspring adiposity, blood pressure, and markers of insulin resistance, although effect sizes are modest and confounding by shared genetics and environment remains a key limitation. Mechanistic data from animal models support sperm-mediated epigenetic pathways linking paternal metabolic status to offspring metabolic programming, yet human epigenetic evidence is inconsistent. At the same time, the widespread use of modern obesity pharmacotherapies, including glucagon-like peptide-1 receptor agonists and dual incretin agonists, has introduced a largely unexamined dimension of paternal exposure. Current data on paternal use of these agents and long-term offspring metabolic outcomes are sparse and fragmentary. As obesity pharmacotherapy expands among men of reproductive age, a shift beyond maternal-only frameworks is warranted. Rigorous studies integrating paternal metabolic profiling, medication exposure, and long-term offspring follow-up are urgently needed to inform clinical practice and public health guidance.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101743"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-10DOI: 10.1016/j.diabet.2026.101741
Yan Chen , Min Yin , Yuting Xie , Chao Deng , Zhiguo Xie , Gan Huang , Shuoming Luo , Zhiguang Zhou , Xia Li
Aims
Antibody-negative type 1 diabetes (T1D) is a provisional diagnosis with unclear etiology. This study aimed to determine the prevalence and phenotypic characteristics of monogenic diabetes within a large antibody-negative T1D cohort.
Methods
A total of 482 antibody-negative T1D patients were included from a clinically diagnosed T1D cohort. Targeted sequencing using a custom gene panel covering 36 genes and the mitochondrial 3243 A > G mutation was performed. Demographic, metabolic, and human leukocyte antigen (HLA) data were analyzed. Beta-cell function was assessed in patients with monogenic diabetes amenable to precision treatment.
Results
Among 482 antibody-negative T1D patients, 2.5% (12/482) had maturity-onset diabetes of the young (MODY) and 1.7% (8/482) had mitochondrial diabetes. The prevalence of MODY increased to 11.1% (6/54) among childhood-onset patients with a single susceptible HLA haplotype, while mitochondrial diabetes reached 6.2% (7/113) in adult-onset patients lacking HLA-susceptible haplotypes. Other characteristics, including gender, age at diagnosis, hemoglobin A1c, 2-hour postprandial C-peptide (2hCP), and family history of diabetes, showed no significant differences. Compared with the “truly” antibody-negative T1D group, MODY patients had an earlier onset, whereas mitochondrial diabetes patients had later onset, higher 2hCP, and fewer HLA-susceptible haplotypes (all P < 0.05). Of eight recalled monogenic diabetes patients, 62.5% (5/8) retained random C-peptide > 100 pmol/L after a median 15.7 years.
Conclusions
In antibody-negative T1D, MODY and mitochondrial diabetes accounted for 2.5% and 1.7%, respectively. HLA genotype was the key distinguishing factor. Persistent C-peptide secretion in monogenic diabetes supports the need for genetic screening in antibody-negative T1D patients.
目的：抗体阴性的1型糖尿病（T1D）是一种病因不明的临时诊断。本研究旨在确定抗体阴性T1D队列中单基因糖尿病的患病率和表型特征。方法：从临床诊断为T1D的队列中共纳入482例抗体阴性的T1D患者。使用包含36个基因和线粒体3243 a > G突变的定制基因面板进行靶向测序。分析人口统计学、代谢和人白细胞抗原（HLA）数据。对可接受精确治疗的单基因糖尿病患者进行β细胞功能评估。结果：在482例抗体阴性T1D患者中，2.5%（12/482）为成熟型糖尿病（MODY）， 1.7%（8/482）为线粒体糖尿病。在HLA基因型单一易感的儿童期发病患者中，MODY的患病率增加到11.1%(6/54)，而在缺乏HLA易感单倍型的成年发病患者中，线粒体糖尿病的患病率达到6.2%（7/113）。其他特征，包括性别、诊断年龄、糖化血红蛋白、餐后2小时c肽（2hCP）、糖尿病家族史，均无显著差异。与“真正”抗体阴性的T1D组相比，MODY患者发病更早，而线粒体糖尿病患者发病更晚，2hCP更高，hla易感单倍型更少（均P < 0.05）。在8名被召回的单基因糖尿病患者中，62.5%（5/8）在中位15.7年后仍保留随机c肽bbb100 pmol/l。结论：在抗体阴性T1D中，MODY和线粒体糖尿病分别占2.5%和1.7%。HLA基因型是关键的区分因素。单基因糖尿病持续c肽分泌支持对抗体阴性T1D患者进行遗传筛查的必要性。
{"title":"HLA-guided identification of monogenic diabetes in antibody-negative type 1 diabetes: frequency and characteristics","authors":"Yan Chen , Min Yin , Yuting Xie , Chao Deng , Zhiguo Xie , Gan Huang , Shuoming Luo , Zhiguang Zhou , Xia Li","doi":"10.1016/j.diabet.2026.101741","DOIUrl":"10.1016/j.diabet.2026.101741","url":null,"abstract":"<div><h3>Aims</h3><div>Antibody-negative type 1 diabetes (T1D) is a provisional diagnosis with unclear etiology. This study aimed to determine the prevalence and phenotypic characteristics of monogenic diabetes within a large antibody-negative T1D cohort.</div></div><div><h3>Methods</h3><div>A total of 482 antibody-negative T1D patients were included from a clinically diagnosed T1D cohort. Targeted sequencing using a custom gene panel covering 36 genes and the mitochondrial 3243 <em>A</em> > <em>G</em> mutation was performed. Demographic, metabolic, and human leukocyte antigen (HLA) data were analyzed. Beta-cell function was assessed in patients with monogenic diabetes amenable to precision treatment.</div></div><div><h3>Results</h3><div>Among 482 antibody-negative T1D patients, 2.5% (12/482) had maturity-onset diabetes of the young (MODY) and 1.7% (8/482) had mitochondrial diabetes. The prevalence of MODY increased to 11.1% (6/54) among childhood-onset patients with a single susceptible HLA haplotype, while mitochondrial diabetes reached 6.2% (7/113) in adult-onset patients lacking HLA-susceptible haplotypes. Other characteristics, including gender, age at diagnosis, hemoglobin A1c, 2-hour postprandial C-peptide (2hCP), and family history of diabetes, showed no significant differences. Compared with the “truly” antibody-negative T1D group, MODY patients had an earlier onset, whereas mitochondrial diabetes patients had later onset, higher 2hCP, and fewer HLA-susceptible haplotypes (all <em>P</em> < 0.05). Of eight recalled monogenic diabetes patients, 62.5% (5/8) retained random C-peptide > 100 pmol/L after a median 15.7 years.</div></div><div><h3>Conclusions</h3><div>In antibody-negative T1D, MODY and mitochondrial diabetes accounted for 2.5% and 1.7%, respectively. HLA genotype was the key distinguishing factor. Persistent C-peptide secretion in monogenic diabetes supports the need for genetic screening in antibody-negative T1D patients.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101741"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146184075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To assessed hyperglycaemia in pregnancy (HIP) prevalence trends over the past decade, accounting for risk factors and screening practices (France introduced early risk-based HIP screening in 2010).
Methods
We analysed national delivery data from the French National Health Data System (SNDS) (2012-2022), excluding women with pre-existing diabetes (n=8,172,911). Poisson regressions with generalized estimating equations estimated prevalence ratios (PR) for HIP risk factors. Counterfactual scenarios quantified contributions of maternal age, early screening, and pre-pregnancy overweight to HIP increase.
Results
HIP prevalence increased from 7.5% in 2012 to 15.7% in 2022, with early HIP tripling. Prevalence rose in 2020–2021 during the Covid-19 pandemic. After adjustment for maternal age, parity, socioeconomic status, season of pregnancy onset, place of delivery, regional prevalence of pre-pregnancy overweight, and early screening, the aPR were 1.30 [1.11–1.51] in 2021 and 1.15 [0.97–1.36] in 2022 vs. 2012 (unadjusted: 2.24 [2.22–2.26] and 2.08 [2.06–2.10]), suggesting that these factors account for a large proportion of the observed increase. While the observed increase in HIP prevalence was 8.2 percentage points from 2012 to 2022, counterfactual scenarios estimated increases of 6.5 [5.9–7.3] for constant maternal age, 6.2 [5.1–7.7] for constant early screening (13.7%), and 4.3 [2.4–5.9] for constant regional pre-pregnancy overweight (11.8%) at 2012 levels.
Conclusion
Rising maternal age, increased early HIP screening, and higher regional pre-pregnancy overweight prevalence mostly contributed to HIP prevalence increase. Public health strategies should prioritize modifiable risk factors—particularly pre-pregnancy overweight—and evaluate the effectiveness of early screening practices.
{"title":"Factors impacting the recent doubling of French hyperglycaemia prevalence in pregnancy","authors":"Élodie Lebreton , Luveon Tang , Sandrine Fosse-Edorh , Anne Vambergue , Emmanuel Cosson , Nolwenn Regnault","doi":"10.1016/j.diabet.2026.101724","DOIUrl":"10.1016/j.diabet.2026.101724","url":null,"abstract":"<div><h3>Aim</h3><div>To assessed hyperglycaemia in pregnancy (HIP) prevalence trends over the past decade, accounting for risk factors and screening practices (France introduced early risk-based HIP screening in 2010).</div></div><div><h3>Methods</h3><div>We analysed national delivery data from the French National Health Data System (SNDS) (2012-2022), excluding women with pre-existing diabetes (n=8,172,911). Poisson regressions with generalized estimating equations estimated prevalence ratios (PR) for HIP risk factors. Counterfactual scenarios quantified contributions of maternal age, early screening, and pre-pregnancy overweight to HIP increase.</div></div><div><h3>Results</h3><div>HIP prevalence increased from 7.5% in 2012 to 15.7% in 2022, with early HIP tripling. Prevalence rose in 2020–2021 during the Covid-19 pandemic. After adjustment for maternal age, parity, socioeconomic status, season of pregnancy onset, place of delivery, regional prevalence of pre-pregnancy overweight, and early screening, the aPR were 1.30 [1.11–1.51] in 2021 and 1.15 [0.97–1.36] in 2022 vs. 2012 (unadjusted: 2.24 [2.22–2.26] and 2.08 [2.06–2.10]), suggesting that these factors account for a large proportion of the observed increase. While the observed increase in HIP prevalence was 8.2 percentage points from 2012 to 2022, counterfactual scenarios estimated increases of 6.5 [5.9–7.3] for constant maternal age, 6.2 [5.1–7.7] for constant early screening (13.7%), and 4.3 [2.4–5.9] for constant regional pre-pregnancy overweight (11.8%) at 2012 levels.</div></div><div><h3>Conclusion</h3><div>Rising maternal age, increased early HIP screening, and higher regional pre-pregnancy overweight prevalence mostly contributed to HIP prevalence increase. Public health strategies should prioritize modifiable risk factors—particularly pre-pregnancy overweight—and evaluate the effectiveness of early screening practices.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101724"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145948848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To evaluate whether GLP-1 RA therapy is associated with an increased risk of NAION in a large, diverse real-world population.
Methods
This retrospective cohort study utilized the TriNetX U.S. Collaborative Network from 2015 to 2024. Adults (≥18 years) with type 2 diabetes mellitus (T2DM) were identified and grouped as GLP-1 RA users versus other antidiabetic users and GLP-1 RA users versus sodium-glucose cotransporter-2 inhibitors (SGLT-2 i) users. Patients with preexisting optic neuropathy or severe ocular disease were excluded. Propensity score matching (1:1) was applied to balance baseline characteristics. The primary outcome was incident NAION, defined by ICD-10 codes. Cox proportional hazards models and Kaplan–Meier analyses were used to estimate hazard ratios (HRs) and cumulative probabilities.
Results
After matching, 799 036 GLP-1 RA users were compared with 799 036 other antidiabetic users, and 429 985 GLP-1 RA users were compared with 429 985 SGLT-2i users. Over 9 years, GLP-1 RA users showed higher cumulative NAION incidence vs other agents (0.21% vs 0.17%; HR 1.38; 95% CI, 1.23–1.55) and vs SGLT-2i users (0.20% vs 0.20%; HR 1.30; 95% CI, 1.11–1.52). Kaplan–Meier curves demonstrated consistent early separation favoring higher risk among GLP-1 RA users. Sensitivity analyses yielded similar patterns.
Conclusions
GLP-1 RA therapy was associated with a modest but statistically significant increased risk of NAION. While the absolute risk remains low, clinicians should consider ophthalmic risk assessment—particularly in patients with anatomical susceptibility or vascular risk factors—as GLP-1 RA use expands for diabetes and obesity management. Further mechanistic and prospective research is warranted.
{"title":"Glucagon-like peptide-1 receptor agonists and the risk of nonarteritic anterior ischemic optic neuropathy: Evidence from a global real-world cohort","authors":"Jun-Wei Chen , Frederick Tzu-En Yu , Hsin-An Chen , Tzu-Fu Huang , Harn-Shen Chen , Tzu-En Wu","doi":"10.1016/j.diabet.2026.101740","DOIUrl":"10.1016/j.diabet.2026.101740","url":null,"abstract":"<div><h3>Aims</h3><div>To evaluate whether GLP-1 RA therapy is associated with an increased risk of NAION in a large, diverse real-world population.</div></div><div><h3>Methods</h3><div>This retrospective cohort study utilized the TriNetX U.S. Collaborative Network from 2015 to 2024. Adults (≥18 years) with type 2 diabetes mellitus (T2DM) were identified and grouped as GLP-1 RA users versus other antidiabetic users and GLP-1 RA users versus sodium-glucose cotransporter-2 inhibitors (SGLT-2 i) users. Patients with preexisting optic neuropathy or severe ocular disease were excluded. Propensity score matching (1:1) was applied to balance baseline characteristics. The primary outcome was incident NAION, defined by ICD-10 codes. Cox proportional hazards models and Kaplan–Meier analyses were used to estimate hazard ratios (HRs) and cumulative probabilities.</div></div><div><h3>Results</h3><div>After matching, 799 036 GLP-1 RA users were compared with 799 036 other antidiabetic users, and 429 985 GLP-1 RA users were compared with 429 985 SGLT-2i users. Over 9 years, GLP-1 RA users showed higher cumulative NAION incidence vs other agents (0.21% vs 0.17%; HR 1.38; 95% CI, 1.23–1.55) and vs SGLT-2i users (0.20% vs 0.20%; HR 1.30; 95% CI, 1.11–1.52). Kaplan–Meier curves demonstrated consistent early separation favoring higher risk among GLP-1 RA users. Sensitivity analyses yielded similar patterns.</div></div><div><h3>Conclusions</h3><div>GLP-1 RA therapy was associated with a modest but statistically significant increased risk of NAION. While the absolute risk remains low, clinicians should consider ophthalmic risk assessment—particularly in patients with anatomical susceptibility or vascular risk factors—as GLP-1 RA use expands for diabetes and obesity management. Further mechanistic and prospective research is warranted.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101740"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146195584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-02DOI: 10.1016/j.diabet.2026.101738
Tzu-Min Lin , Tzu-Ching Lin , Cheng-Han Lin , Chih-Sheng Lin
Stem cell–based therapies are a leading frontier in diabetes treatment, aiming to restore insulin-producing β-cell function beyond symptomatic management. Clinical progress has evolved from donor islet transplantation, such as the Edmonton Protocol, to pluripotent stem cell–derived β-cell replacement. Embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) can differentiate into insulin-producing cells, while mesenchymal stem cells (MSCs) provide immunomodulatory and metabolic support. Landmark trials by ViaCyte, Vertex, and Sernova tested ESCs- and iPSCs-derived progenitors with encapsulation devices and bioengineered niches, yielding insights into safety, differentiation, and immune responses. Vertex’s VX-880 program achieved insulin independence, and a 2024 Cell study reported the first functional cure of type 1 diabetes using chemical induced iPSCs (CiPSCs)-derived islets. Encapsulation technologies dominate trials, aiming to shield transplanted cells from rejection without systemic immunosuppression, though fibrosis and vascularization remain obstacles. MSCs therapies across Phase 1–3 trials improved glycemic control and β-cell preservation, underscoring their complementary role. Despite promising outcomes, no clinical stem cell–derived therapy is yet routine, with tumorigenicity, immune rejection, and scalability as key challenges. Future directions focus on gene-edited immune-evasive cells, advanced biomaterials, scalable bioreactors, and harmonized regulation to achieve durable insulin independence and global accessibility.
{"title":"Overview of the major clinical trials investigating stem cells–based therapies for diabetes","authors":"Tzu-Min Lin , Tzu-Ching Lin , Cheng-Han Lin , Chih-Sheng Lin","doi":"10.1016/j.diabet.2026.101738","DOIUrl":"10.1016/j.diabet.2026.101738","url":null,"abstract":"<div><div>Stem cell–based therapies are a leading frontier in diabetes treatment, aiming to restore insulin-producing β-cell function beyond symptomatic management. Clinical progress has evolved from donor islet transplantation, such as the Edmonton Protocol, to pluripotent stem cell–derived β-cell replacement. Embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) can differentiate into insulin-producing cells, while mesenchymal stem cells (MSCs) provide immunomodulatory and metabolic support. Landmark trials by ViaCyte, Vertex, and Sernova tested ESCs- and iPSCs-derived progenitors with encapsulation devices and bioengineered niches, yielding insights into safety, differentiation, and immune responses. Vertex’s VX-880 program achieved insulin independence, and a 2024 Cell study reported the first functional cure of type 1 diabetes using chemical induced iPSCs (CiPSCs)-derived islets. Encapsulation technologies dominate trials, aiming to shield transplanted cells from rejection without systemic immunosuppression, though fibrosis and vascularization remain obstacles. MSCs therapies across Phase 1–3 trials improved glycemic control and β-cell preservation, underscoring their complementary role. Despite promising outcomes, no clinical stem cell–derived therapy is yet routine, with tumorigenicity, immune rejection, and scalability as key challenges. Future directions focus on gene-edited immune-evasive cells, advanced biomaterials, scalable bioreactors, and harmonized regulation to achieve durable insulin independence and global accessibility.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101738"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146121620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-06DOI: 10.1016/j.diabet.2026.101725
Benjamin Bouillet , Romain Boulestreau , Victor Aboyans , Sophie Béliard , Franck Boccara , Bertrand Cariou , Sybil Charrière , Philippe Moulin , Bruno Vergès , Rene Valero , Antonio Gallo
{"title":"Management of dyslipidemia in adults. A consensus statement from the French Society of Endocrinology (SFE), the French-speaking Diabetes Society (SFD), the New French-speaking Atherosclerosis Society (NSFA) and the French Society of Cardiology (SFC)","authors":"Benjamin Bouillet , Romain Boulestreau , Victor Aboyans , Sophie Béliard , Franck Boccara , Bertrand Cariou , Sybil Charrière , Philippe Moulin , Bruno Vergès , Rene Valero , Antonio Gallo","doi":"10.1016/j.diabet.2026.101725","DOIUrl":"10.1016/j.diabet.2026.101725","url":null,"abstract":"","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101725"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-15DOI: 10.1016/j.diabet.2026.101729
Siyu Sun , Siqian Gong , Tianhao Ba , Meng Li , Wei Liu , Rui Zhang , Yumin Ma , Fang Wang , Xiaoling Cai , Yingying Luo , Simin Zhang , Lingli Zhou , Yu Zhu , Xiuying Zhang , Jing Chen , Ling Chen , Jing Wu , Leili Gao , Xianghai Zhou , Liyong Zhong , Linong Ji
Aim
Monogenic diabetes is a group of disorders arising from single gene mutations with a clear pathophysiology, most of which present with impaired beta cell function rather than insulin resistance. This study aims to evaluate the ability of TyG index and polygenetic risk score (PRS) to identify multi-type beta cell monogenetic diabetes (beta-cell-MgD) in Chinese early-onset type 2 diabetes (EOD) population.
Methods
A prediction model for beta-cell-MgD was established by logistic regression analysis in Cohort 1 (92 beta-cell-MgD, 512 EOD). Model performance was evaluated by receiver operating characteristic curves (ROC) and validated in an independent case-control sample (Cohort 2, 35 beta-cell-MgD, 50 EOD) and a newly diagnosed drug-naive EOD cohort (Cohort 3, 7 beta-cell-MgD, 176 EOD). PRS was constructed based on Genome-wide genotyping data from participants in Cohort 3. The ability of PRS to identify beta-cell-MgD was tested by ROC.
Results
The TyG-MgD score based on age at diagnosis, BMI and TyG presented a good performance to distinguish beta-cell-MgD (AUC=0.769), and achieving AUCs of 0.966 and 0.754 respectively in validation cohorts. At the optimal cutoff point -16.19, the model achieved a sensitivity of 66.3% and a specificity of 75.39%, allowing one case of beta-cell-MgD identified among every three patients. -16.85 could be used as the screening threshold prioritizing 80% sensitivity (with 59% specificity). Models combining TyG-MgD with East Asian PRS and beta-cell dysfunction-high proinsulin partitioned polygenetic score showed AUCs of 0.842 and 0.834 respectively for indentifying beta-cell-MgD.
Conclusion
We developed a clinical prediction model as a simple screening tool for multi-type beta-cell-MgD, identifying who are most likely to benefit from next genetic sequencing in Chinese population. PRS might be helpful for further screening of MgD.
{"title":"A clinical prediction model for beta cell monogenetic diabetes in Chinese patients with early-onset type 2 diabetes","authors":"Siyu Sun , Siqian Gong , Tianhao Ba , Meng Li , Wei Liu , Rui Zhang , Yumin Ma , Fang Wang , Xiaoling Cai , Yingying Luo , Simin Zhang , Lingli Zhou , Yu Zhu , Xiuying Zhang , Jing Chen , Ling Chen , Jing Wu , Leili Gao , Xianghai Zhou , Liyong Zhong , Linong Ji","doi":"10.1016/j.diabet.2026.101729","DOIUrl":"10.1016/j.diabet.2026.101729","url":null,"abstract":"<div><h3>Aim</h3><div>Monogenic diabetes is a group of disorders arising from single gene mutations with a clear pathophysiology, most of which present with impaired beta cell function rather than insulin resistance. This study aims to evaluate the ability of TyG index and polygenetic risk score (PRS) to identify multi-type beta cell monogenetic diabetes (beta-cell-MgD) in Chinese early-onset type 2 diabetes (EOD) population.</div></div><div><h3>Methods</h3><div>A prediction model for beta-cell-MgD was established by logistic regression analysis in Cohort 1 (92 beta-cell-MgD, 512 EOD). Model performance was evaluated by receiver operating characteristic curves (ROC) and validated in an independent case-control sample (Cohort 2, 35 beta-cell-MgD, 50 EOD) and a newly diagnosed drug-naive EOD cohort (Cohort 3, 7 beta-cell-MgD, 176 EOD). PRS was constructed based on Genome-wide genotyping data from participants in Cohort 3. The ability of PRS to identify beta-cell-MgD was tested by ROC.</div></div><div><h3>Results</h3><div>The TyG-MgD score based on age at diagnosis, BMI and TyG presented a good performance to distinguish beta-cell-MgD (AUC=0.769), and achieving AUCs of 0.966 and 0.754 respectively in validation cohorts. At the optimal cutoff point -16.19, the model achieved a sensitivity of 66.3% and a specificity of 75.39%, allowing one case of beta-cell-MgD identified among every three patients. -16.85 could be used as the screening threshold prioritizing 80% sensitivity (with 59% specificity). Models combining TyG-MgD with East Asian PRS and beta-cell dysfunction-high proinsulin partitioned polygenetic score showed AUCs of 0.842 and 0.834 respectively for indentifying beta-cell-MgD.</div></div><div><h3>Conclusion</h3><div>We developed a clinical prediction model as a simple screening tool for multi-type beta-cell-MgD, identifying who are most likely to benefit from next genetic sequencing in Chinese population. PRS might be helpful for further screening of MgD.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"52 2","pages":"Article 101729"},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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