Pub Date : 2025-04-21DOI: 10.1016/j.diabet.2025.101655
Mingyang Sun , Xiaoling Wang , Zhongyuan Lu , Yitian Yang , Shuang Lv , Mengrong Miao , Wan-Ming Chen , Szu-Yuan Wu , Jiaqiang Zhang
Background
- Type 2 diabetes (T2D) increases the risk of dementia by 1.5 to 2.5 times. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) and metformin, widely used antidiabetic therapies, have demonstrated potential neuroprotective effects. Their comparative effectiveness in dementia prevention remains unknown.
Methods
- This retrospective cohort study used the TriNetX global federated network, analyzing de-identified records from over 98 healthcare organizations. Adults with T2D initiating SGLT2i or metformin as first-line therapy were propensity score-matched (1:1). The primary outcome was overall dementia incidence, including vascular dementia, Alzheimer’s disease, and other subtypes. Secondary outcomes included all-cause mortality. Time-to-event outcomes were assessed using Kaplan-Meier curves and Cox models.
Results
- Among 74,975 matched patients in each cohort, SGLT2i use was associated with a lower incidence of overall dementia: 2.7 % vs. 6.9 %: adjusted hazard ratio (aHR) 0.80 [95 % CI 0.76;0.84]. Reductions were observed in vascular dementia (0.8 % vs. 2.0 %; aHR 0.87), Alzheimer’s dementia (1.1 % vs. 3.2 %; aHR, 0.76), and all-cause mortality (6.8 % vs. 15.4 %; aHR, 0.92). Benefits were pronounced in older adults, particularly those aged ≥80 years.
Conclusions
- SGLT2is significantly reduced dementia risk and mortality compared to metformin in T2D patients. These findings suggest SGLT2is may offer superior neuroprotective benefits, underscoring their potential as a first-line therapy for T2D. Further randomized trials are needed to confirm these results.
背景- 2型糖尿病（T2D）使痴呆的风险增加1.5至2.5倍。钠-葡萄糖共转运蛋白2抑制剂（SGLT2is）和二甲双胍，广泛应用于降糖治疗，已显示出潜在的神经保护作用。它们在预防痴呆症方面的相对有效性尚不清楚。方法：这项回顾性队列研究使用TriNetX全球联合网络，分析了来自98个医疗保健组织的去识别记录。成人t2dm患者采用SGLT2i或二甲双胍作为一线治疗，倾向评分匹配（1:1）。主要结局是总体痴呆发病率，包括血管性痴呆、阿尔茨海默病和其他亚型。次要结局包括全因死亡率。使用Kaplan-Meier曲线和Cox模型评估事件发生时间。结果：在每个队列的74,975名匹配的患者中，SGLT2i的使用与较低的总体痴呆发病率相关：2.7% vs. 6.9%：校正风险比（aHR） 0.80 [95% CI 0.76;0.84]。血管性痴呆减少(0.8% vs. 2.0%；aHR 0.87)，阿尔茨海默氏痴呆(1.1%对3.2%；aHR, 0.76)和全因死亡率(6.8% vs. 15.4%；aHR, 0.92)。在老年人中获益明显，尤其是年龄≥80岁的老年人。结论：与二甲双胍相比，sglt2dm可显著降低T2D患者的痴呆风险和死亡率。这些发现表明SGLT2is可能具有更好的神经保护作用，强调了它们作为T2D一线治疗的潜力。需要进一步的随机试验来证实这些结果。
{"title":"Comparative study of SGLT2 inhibitors and metformin: Evaluating first-line therapies for dementia prevention in type 2 diabetes","authors":"Mingyang Sun , Xiaoling Wang , Zhongyuan Lu , Yitian Yang , Shuang Lv , Mengrong Miao , Wan-Ming Chen , Szu-Yuan Wu , Jiaqiang Zhang","doi":"10.1016/j.diabet.2025.101655","DOIUrl":"10.1016/j.diabet.2025.101655","url":null,"abstract":"<div><h3>Background</h3><div><em>-</em> Type 2 diabetes (T2D) increases the risk of dementia by 1.5 to 2.5 times. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) and metformin, widely used antidiabetic therapies, have demonstrated potential neuroprotective effects. Their comparative effectiveness in dementia prevention remains unknown.</div></div><div><h3>Methods</h3><div><em>-</em> This retrospective cohort study used the TriNetX global federated network, analyzing de-identified records from over 98 healthcare organizations. Adults with T2D initiating SGLT2i or metformin as first-line therapy were propensity score-matched (1:1). The primary outcome was overall dementia incidence, including vascular dementia, Alzheimer’s disease, and other subtypes. Secondary outcomes included all-cause mortality. Time-to-event outcomes were assessed using Kaplan-Meier curves and Cox models.</div></div><div><h3>Results</h3><div><em>-</em> Among 74,975 matched patients in each cohort, SGLT2i use was associated with a lower incidence of overall dementia: 2.7 % vs. 6.9 %: adjusted hazard ratio (aHR) 0.80 [95 % CI 0.76;0.84]. Reductions were observed in vascular dementia (0.8 % vs. 2.0 %; aHR 0.87), Alzheimer’s dementia (1.1 % vs. 3.2 %; aHR, 0.76), and all-cause mortality (6.8 % vs. 15.4 %; aHR, 0.92). Benefits were pronounced in older adults, particularly those aged ≥80 years.</div></div><div><h3>Conclusions</h3><div><em>-</em> SGLT2is significantly reduced dementia risk and mortality compared to metformin in T2D patients. These findings suggest SGLT2is may offer superior neuroprotective benefits, underscoring their potential as a first-line therapy for T2D. Further randomized trials are needed to confirm these results.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 4","pages":"Article 101655"},"PeriodicalIF":4.6,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899449","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}
Patients living with highly unstable type 1 diabetes (T1D) are eligible for beta-cell replacement (βCR) therapy (islet or pancreas transplantation). This study aimed to evaluate glycemic control in patients treated with automated insulin delivery (AID) following failed βCR therapy, defined as secondary graft failure or marginal function.
Material and Methods
A national, multicenter, retrospective study was conducted with 23 patients who had βCR failure treated with AID for at least three months. The primary outcome was the proportion of patients achieving recommended glucose targets (time in 70–180mg/dl range [TIR] > 70 %, time below range [TBR] < 4 % and HbA1c < 7 %). Secondary outcomes included TIR, glycemia risk index (GRI), HbA1c, coefficient of variation (CV), body weight, insulin doses, severe hypoglycemia and AID discontinuation.
Results
The proportion of patients achieving recommended glucose targets under AID increased from 5.0 % to 57.1 % after 12 months. TIR increased from 54.2 ± 18.0 % to 75.5 ± 9.6 % after 12-month AID, while GRI decreased from 45.8 ± 22.2 % to 25.6 ± 10.3 %. HbA1c levels decreased from 7.5 ± 0.9 % to 7.0 ± 1.1 % after 12-month AID. CV, body weight and insulin doses did not change. All patients were free from severe hypoglycemia under AID, including those who had experienced severe hypoglycemia after βCR failure. No patient discontinued the AID.
Conclusions
This study highlights the effectiveness of AID in achieving glucose control targets and preventing severe hypoglycemia in patients with T1D following βCR failure. AID may serve as a valuable therapeutic option to improve glucose control when graft function declines.
{"title":"Automated insulin delivery after beta-cell replacement failure in people living with type 1 diabetes","authors":"Quentin Perrier , Sandrine Lablanche , Luc Rakotoarisoa , Orianne Villard , Jean-Pierre Riveline , Jean-Baptiste Julla , Fanny Buron , Sophie Reffet , Eric Renard , Laurence Kessler , Pierre-Yves Benhamou","doi":"10.1016/j.diabet.2025.101654","DOIUrl":"10.1016/j.diabet.2025.101654","url":null,"abstract":"<div><h3>Aims</h3><div>Patients living with highly unstable type 1 diabetes (T1D) are eligible for beta-cell replacement (βCR) therapy (islet or pancreas transplantation). This study aimed to evaluate glycemic control in patients treated with automated insulin delivery (AID) following failed βCR therapy, defined as secondary graft failure or marginal function.</div></div><div><h3>Material and Methods</h3><div>A national, multicenter, retrospective study was conducted with 23 patients who had βCR failure treated with AID for at least three months. The primary outcome was the proportion of patients achieving recommended glucose targets (time in 70–180mg/dl range [TIR] > 70 %, time below range [TBR] < 4 % and HbA1c < 7 %). Secondary outcomes included TIR, glycemia risk index (GRI), HbA1c, coefficient of variation (CV), body weight, insulin doses, severe hypoglycemia and AID discontinuation.</div></div><div><h3>Results</h3><div>The proportion of patients achieving recommended glucose targets under AID increased from 5.0 % to 57.1 % after 12 months. TIR increased from 54.2 ± 18.0 % to 75.5 ± 9.6 % after 12-month AID, while GRI decreased from 45.8 ± 22.2 % to 25.6 ± 10.3 %. HbA1c levels decreased from 7.5 ± 0.9 % to 7.0 ± 1.1 % after 12-month AID. CV, body weight and insulin doses did not change. All patients were free from severe hypoglycemia under AID, including those who had experienced severe hypoglycemia after βCR failure. No patient discontinued the AID.</div></div><div><h3>Conclusions</h3><div>This study highlights the effectiveness of AID in achieving glucose control targets and preventing severe hypoglycemia in patients with T1D following βCR failure. AID may serve as a valuable therapeutic option to improve glucose control when graft function declines.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 4","pages":"Article 101654"},"PeriodicalIF":4.6,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143877476","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 : 2025-04-18DOI: 10.1016/j.diabet.2025.101653
Yan Liu , Kaihui Ma , Aiying Zhang , Yun Cui , Hui Zhao , Xinhua Li , Ke Zhao
Aim
Fatty acid-binding protein 4 (FABP4) is associated with the risk of developing diabetes and its microvascular complications. We aimed to explore the association between serum FABP4 levels and the risk of diabetic retinopathy (DR) in patients with type 2 diabetes mellitus (T2DM).
Methods
Serum FABP4 levels were measured via enzyme-linked immunosorbent assay in 275 individuals (78 healthy controls, 197 T2DM patients). DR severity was determined via fundus fluorescence angiography. Multivariate analyses were performed via logistic regression models. The diagnostic value of these measures was assessed via receiver operating characteristic curve analysis.
Results
Serum FABP4 levels were significantly greater in the proliferative DR (PDR) group than in the ZeroDR (ZDR) and non-proliferative DR (NPDR) groups, and the FABP4 levels positively with DR severity (r = 0.328, P < 0.001). Logistic regression analysis revealed that after adjusting for potential confounders, increased FABP4, fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c) levels were risk factors for DR development, and FABP4 was an independent risk factor for PDR development. A multivariate logistic regression model that included FABP4 as a categorical binary variable with a cutoff value of 20.57 ng/ml revealed that a level of FABP4 above the cutoff value increased the DR risk (OR=6.394; 95 % CI=3.18;13.58; P < 0.001). Similarly, a FABP4 concentration above the cutoff value of 24.40 ng/ml increased the PDR risk (OR=4.686; 95 % CI=1.907;12.34; P = 0.001).
Conclusion
The FABP4 level is associated with DR severity and has the potential as a serum biomarker for DR prediction.
脂肪酸结合蛋白4 （FABP4）与糖尿病及其微血管并发症的发生风险相关。我们旨在探讨血清FABP4水平与2型糖尿病（T2DM）患者糖尿病视网膜病变（DR）风险之间的关系。方法采用酶联免疫吸附法测定275例（健康对照78例，T2DM患者197例）血清FABP4水平。通过眼底荧光血管造影确定DR严重程度。通过logistic回归模型进行多变量分析。通过受试者工作特征曲线分析评估这些指标的诊断价值。结果增殖性DR （PDR）组血清FABP4水平显著高于无增殖性DR （ZDR）和非增殖性DR （NPDR）组，且与DR严重程度呈正相关(r = 0.328, P <；0.001)。Logistic回归分析显示，在调整潜在混杂因素后，FABP4、空腹血糖（FPG）和血红蛋白A1c （HbA1c）水平升高是DR发生的危险因素，FABP4是PDR发生的独立危险因素。将FABP4作为分类二元变量（截断值为20.57 ng/ml）的多因素logistic回归模型显示，高于截断值的FABP4水平增加了DR风险(OR=6.394；95% ci =3.18;13.58；P & lt;0.001)。同样，高于临界值24.40 ng/ml的FABP4浓度会增加PDR风险(OR=4.686；95% ci =1.907;12.34；P = 0.001)。结论FABP4水平与DR严重程度相关，可作为预测DR的血清生物标志物。
{"title":"Increased fatty acid-binding protein 4 levels are associated with the risk of developing retinopathy in type 2 diabetes mellitus patients","authors":"Yan Liu , Kaihui Ma , Aiying Zhang , Yun Cui , Hui Zhao , Xinhua Li , Ke Zhao","doi":"10.1016/j.diabet.2025.101653","DOIUrl":"10.1016/j.diabet.2025.101653","url":null,"abstract":"<div><h3>Aim</h3><div>Fatty acid-binding protein 4 (FABP4) is associated with the risk of developing diabetes and its microvascular complications. We aimed to explore the association between serum FABP4 levels and the risk of diabetic retinopathy (DR) in patients with type 2 diabetes mellitus (T2DM).</div></div><div><h3>Methods</h3><div>Serum FABP4 levels were measured via enzyme-linked immunosorbent assay in 275 individuals (78 healthy controls, 197 T2DM patients). DR severity was determined via fundus fluorescence angiography. Multivariate analyses were performed via logistic regression models. The diagnostic value of these measures was assessed via receiver operating characteristic curve analysis.</div></div><div><h3>Results</h3><div>Serum FABP4 levels were significantly greater in the proliferative DR (PDR) group than in the ZeroDR (ZDR) and non-proliferative DR (NPDR) groups, and the FABP4 levels positively with DR severity (<em>r</em> = 0.328, <em>P</em> < 0.001). Logistic regression analysis revealed that after adjusting for potential confounders, increased FABP4, fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c) levels were risk factors for DR development, and FABP4 was an independent risk factor for PDR development. A multivariate logistic regression model that included FABP4 as a categorical binary variable with a cutoff value of 20.57 ng/ml revealed that a level of FABP4 above the cutoff value increased the DR risk (OR=6.394; 95 % CI=3.18;13.58; <em>P</em> < 0.001). Similarly, a FABP4 concentration above the cutoff value of 24.40 ng/ml increased the PDR risk (OR=4.686; 95 % CI=1.907;12.34; <em>P</em> = 0.001).</div></div><div><h3>Conclusion</h3><div>The FABP4 level is associated with DR severity and has the potential as a serum biomarker for DR prediction.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 4","pages":"Article 101653"},"PeriodicalIF":4.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143870631","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 : 2025-04-15DOI: 10.1016/j.diabet.2025.101645
Patrick Henry , Sophie Jacqueminet , Gilles Lemesle , Gaetan Prevost , Franck Boccara , Emmanuel Cosson , Etienne Puymirat , Denis Angoulvant , François Roubille , Serge Kownator , Paul Valensi , Victor Aboyans , Bruno Vergès
Patients with type 2 diabetes, but also older patients with type 1 diabetes, are at major risk of cardiovascular morbidity and death. After an acute cardiac event, the prognosis of patients with diabetes is impaired, with clear increases in in-hospital and long-term morbidity and deaths. Both hyper- and hypoglycaemia are deleterious after an acute cardiac event, and the decision to start intravenous insulin is often challenging. Moreover, some antidiabetic treatments have cardioprotective effects, and the onset of an acute cardiac event provides an opportunity to shift to these treatments. The objective of this position statement is to offer practical tools to cardiologists seeking to improve the care of patients with diabetes hospitalized for an acute cardiac event, and to optimize collaboration between cardiologists and diabetologists. After a summary of the evidence for antidiabetic treatments in patients with acute cardiac events, we propose an algorithm to start and adapt intravenous insulin in the most severe patients, and conclude with standard insulin protocols or oral treatments at discharge. We also discuss appropriate antidiabetic treatment of these patients at discharge, based on the main cardiological diagnosis, kidney function and antidiabetic strategies. Finally, situations in which the diabetologist must be consulted are discussed.
{"title":"Management of diabetes in patients hospitalized for acute cardiac events: Joint position paper from the French Society of Cardiology and the French-speaking Diabetes Society","authors":"Patrick Henry , Sophie Jacqueminet , Gilles Lemesle , Gaetan Prevost , Franck Boccara , Emmanuel Cosson , Etienne Puymirat , Denis Angoulvant , François Roubille , Serge Kownator , Paul Valensi , Victor Aboyans , Bruno Vergès","doi":"10.1016/j.diabet.2025.101645","DOIUrl":"10.1016/j.diabet.2025.101645","url":null,"abstract":"<div><div>Patients with type 2 diabetes, but also older patients with type 1 diabetes, are at major risk of cardiovascular morbidity and death. After an acute cardiac event, the prognosis of patients with diabetes is impaired, with clear increases in in-hospital and long-term morbidity and deaths. Both hyper- and hypoglycaemia are deleterious after an acute cardiac event, and the decision to start intravenous insulin is often challenging. Moreover, some antidiabetic treatments have cardioprotective effects, and the onset of an acute cardiac event provides an opportunity to shift to these treatments. The objective of this position statement is to offer practical tools to cardiologists seeking to improve the care of patients with diabetes hospitalized for an acute cardiac event, and to optimize collaboration between cardiologists and diabetologists. After a summary of the evidence for antidiabetic treatments in patients with acute cardiac events, we propose an algorithm to start and adapt intravenous insulin in the most severe patients, and conclude with standard insulin protocols or oral treatments at discharge. We also discuss appropriate antidiabetic treatment of these patients at discharge, based on the main cardiological diagnosis, kidney function and antidiabetic strategies. Finally, situations in which the diabetologist must be consulted are discussed.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 3","pages":"Article 101645"},"PeriodicalIF":4.6,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143883128","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}
Chronic Obstructive Pulmonary Disease (COPD) and Type 2 Diabetes Mellitus (T2DM) often coexist, leading to compounded morbidity, mortality, and healthcare burden. COPD exacerbations significantly impact patients with T2DM, with increased frequency and severity. Sodium-glucose cotransporter-2 inhibitors (SGLT-2i) have demonstrated promising benefits in managing both glycemic control and respiratory health. This systematic review and meta-analysis aim to assess the impact of SGLT-2 inhibitors on COPD exacerbations in T2DM patients.
Methods
We conducted a systematic review and meta-analysis following PRISMA guidelines, evaluating studies published until March 2025. A broad search strategy across PubMed, Embase, and Web of Science identified relevant studies comparing SGLT-2 inhibitors with other antidiabetic agents. Studies meeting predefined eligibility criteria, including those providing quantitative data on COPD exacerbation frequency and hospitalization rates, were included in the analysis.
Results
Eight studies involving 4,64,542 participants were included. The pooled hazard ratio (HR) for the impact of SGLT-2 inhibitors on COPD exacerbations was 0.646 (95 % CI: 0.470–0.889), demonstrating a 35 % decrease in exacerbations compared to other antidiabetic agents. SGLT-2 inhibitors demonstrated superior efficacy over DPP-4 inhibitors (HR: 0.618, 95 % CI: 0.462–0.827) and sulfonylureas (HR: 0.620, 95 % CI: 0.526–0.731). However, the reduction in severe exacerbations was not statistically significant (HR: 0.715, 95 % CI: 0.403–1.269). Subgroup analysis indicated that SGLT-2 inhibitors had a modest but significant advantage over GLP-1 receptor agonists (HR: 0.940, 95 % CI: 0.890–0.993).
Conclusions
SGLT-2 inhibitors significantly reduce COPD exacerbations in T2DM patients, offering dual benefits in managing both glycemic control and respiratory health. These findings support the integration of SGLT-2 inhibitors into treatment regimens for T2DM-COPD overlap. Further randomized controlled trials and long-term studies are needed to confirm the lasting efficacy and explore the underlying mechanisms.
{"title":"Impact of SGLT-2i on COPD exacerbations in patients with type 2 diabetes mellitus: A systematic review and meta-analysis","authors":"Prakasini Satapathy , Abhay M Gaidhane , Nasir Vadia , Soumya V Menon , Kattela Chennakesavulu , Rajashree Panigrahi , Jayaraj Patil , Ganesh Bushi , Mahendra Singh , Awakash Turkar , Sanjit Sah , S. Govinda Rao , Khang Wen Goh , Muhammed Shabil","doi":"10.1016/j.diabet.2025.101646","DOIUrl":"10.1016/j.diabet.2025.101646","url":null,"abstract":"<div><h3>Background</h3><div>Chronic Obstructive Pulmonary Disease (COPD) and Type 2 Diabetes Mellitus (T2DM) often coexist, leading to compounded morbidity, mortality, and healthcare burden. COPD exacerbations significantly impact patients with T2DM, with increased frequency and severity. Sodium-glucose cotransporter-2 inhibitors (SGLT-2i) have demonstrated promising benefits in managing both glycemic control and respiratory health. This systematic review and meta-analysis aim to assess the impact of SGLT-2 inhibitors on COPD exacerbations in T2DM patients.</div></div><div><h3>Methods</h3><div>We conducted a systematic review and meta-analysis following PRISMA guidelines, evaluating studies published until March 2025. A broad search strategy across PubMed, Embase, and Web of Science identified relevant studies comparing SGLT-2 inhibitors with other antidiabetic agents. Studies meeting predefined eligibility criteria, including those providing quantitative data on COPD exacerbation frequency and hospitalization rates, were included in the analysis.</div></div><div><h3>Results</h3><div>Eight studies involving 4,64,542 participants were included. The pooled hazard ratio (HR) for the impact of SGLT-2 inhibitors on COPD exacerbations was 0.646 (95 % CI: 0.470–0.889), demonstrating a 35 % decrease in exacerbations compared to other antidiabetic agents. SGLT-2 inhibitors demonstrated superior efficacy over DPP-4 inhibitors (HR: 0.618, 95 % CI: 0.462–0.827) and sulfonylureas (HR: 0.620, 95 % CI: 0.526–0.731). However, the reduction in severe exacerbations was not statistically significant (HR: 0.715, 95 % CI: 0.403–1.269). Subgroup analysis indicated that SGLT-2 inhibitors had a modest but significant advantage over GLP-1 receptor agonists (HR: 0.940, 95 % CI: 0.890–0.993).</div></div><div><h3>Conclusions</h3><div>SGLT-2 inhibitors significantly reduce COPD exacerbations in T2DM patients, offering dual benefits in managing both glycemic control and respiratory health. These findings support the integration of SGLT-2 inhibitors into treatment regimens for T2DM-COPD overlap. Further randomized controlled trials and long-term studies are needed to confirm the lasting efficacy and explore the underlying mechanisms.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 4","pages":"Article 101646"},"PeriodicalIF":4.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843437","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 : 2025-04-04DOI: 10.1016/j.diabet.2025.101644
Audrey Poisson, Patricia Vaduva, Agathe Guenego
{"title":"Open source automated insulin delivery: State of play in France","authors":"Audrey Poisson, Patricia Vaduva, Agathe Guenego","doi":"10.1016/j.diabet.2025.101644","DOIUrl":"10.1016/j.diabet.2025.101644","url":null,"abstract":"","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 4","pages":"Article 101644"},"PeriodicalIF":4.6,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797486","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 : 2025-04-04DOI: 10.1016/j.diabet.2025.101643
Blanca Gómez-Zaragoza , María Ruiz-Rodríguez , Pablo Rodríguez de Vera Gómez , Daniela Decan-Bardasz , María Asunción Martínez-Brocca
We report the case of a 30-year-old male with psoriatic arthritis treated with secukinumab (anti-IL-17A) who developed new-onset type 1 diabetes mellitus (T1DM). During follow-up, a consistent reduction in insulin requirements and glycemic variability was observed in the two weeks following each dose of secukinumab. This suggests a possible immunomodulatory effect of IL-17 inhibition on beta-cell function and glycemic control. To our knowledge, this is the first report describing clinical benefits of secukinumab in the early stages of T1DM, highlighting its potential as a therapeutic tool in modulating autoimmune processes involved in disease progression.
{"title":"Secukinumab (Anti-IL-17) induces clinical regression in early diagnosed type 1 diabetes: A case report","authors":"Blanca Gómez-Zaragoza , María Ruiz-Rodríguez , Pablo Rodríguez de Vera Gómez , Daniela Decan-Bardasz , María Asunción Martínez-Brocca","doi":"10.1016/j.diabet.2025.101643","DOIUrl":"10.1016/j.diabet.2025.101643","url":null,"abstract":"<div><div>We report the case of a 30-year-old male with psoriatic arthritis treated with secukinumab (anti-IL-17A) who developed new-onset type 1 diabetes mellitus (T1DM). During follow-up, a consistent reduction in insulin requirements and glycemic variability was observed in the two weeks following each dose of secukinumab. This suggests a possible immunomodulatory effect of IL-17 inhibition on beta-cell function and glycemic control. To our knowledge, this is the first report describing clinical benefits of secukinumab in the early stages of T1DM, highlighting its potential as a therapeutic tool in modulating autoimmune processes involved in disease progression.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 3","pages":"Article 101643"},"PeriodicalIF":4.6,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797487","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 : 2025-03-28DOI: 10.1016/j.diabet.2025.101642
Coralie Amadou , Alfred Penfornis
{"title":"Automated insulin delivery for people living with Type 1 Diabetes in France: A long road ahead","authors":"Coralie Amadou , Alfred Penfornis","doi":"10.1016/j.diabet.2025.101642","DOIUrl":"10.1016/j.diabet.2025.101642","url":null,"abstract":"","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 3","pages":"Article 101642"},"PeriodicalIF":4.6,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143747212","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 : 2025-03-22DOI: 10.1016/j.diabet.2025.101641
Chen J , Cooper ME , Coughlan MT
Glucagon-like peptide-1 (GLP-1) is an incretin hormone, secreted from gut endocrine cells, which acts to potentiate nutrient-induced insulin secretion. Activation of its receptor, GLP-1R, decreases glucagon secretion and gastric emptying, thereby decreasing blood glucose and body weight. It is largely through these mechanisms that Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have transformed the treatment of type 2 diabetes. More recently, preclinical and clinical studies have reported that these agents have potent extra-pancreatic effects, exhibiting cardioprotective and renoprotective actions. The recent FLOW trial was the first multicentre clinical trial investigating the effect of GLP-1RAs on a primary renal outcome and reported robust evidence that GLP-1RAs are renoprotective. Studies in rodent models of renal injury have shown that gain and loss of GLP-1R signalling improves or deteriorates kidney function. However, the precise mechanisms responsible for renal benefits of GLP-1RAs are not yet fully understood. While prolonged activation of GLP-1 receptors (GLP-1R) has been shown to reverse diabetes-related disruptions in gene expression across various renal cell populations, GLP-1R expression in both rodent and human kidneys is thought to be primarily confined to certain vascular smooth muscle cells. This review discusses recent advances in our understanding of the effects of GLP-1 medicines on the kidney with a focus on indirect and direct mechanisms of action.
{"title":"Renoprotective mechanisms of glucagon-like peptide-1 receptor agonists","authors":"Chen J , Cooper ME , Coughlan MT","doi":"10.1016/j.diabet.2025.101641","DOIUrl":"10.1016/j.diabet.2025.101641","url":null,"abstract":"<div><div>Glucagon-like peptide-1 (GLP-1) is an incretin hormone, secreted from gut endocrine cells, which acts to potentiate nutrient-induced insulin secretion. Activation of its receptor, GLP-1R, decreases glucagon secretion and gastric emptying, thereby decreasing blood glucose and body weight. It is largely through these mechanisms that Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have transformed the treatment of type 2 diabetes. More recently, preclinical and clinical studies have reported that these agents have potent extra-pancreatic effects, exhibiting cardioprotective and renoprotective actions. The recent FLOW trial was the first multicentre clinical trial investigating the effect of GLP-1RAs on a primary renal outcome and reported robust evidence that GLP-1RAs are renoprotective. Studies in rodent models of renal injury have shown that gain and loss of GLP-1R signalling improves or deteriorates kidney function. However, the precise mechanisms responsible for renal benefits of GLP-1RAs are not yet fully understood. While prolonged activation of GLP-1 receptors (GLP-1R) has been shown to reverse diabetes-related disruptions in gene expression across various renal <strong>cell</strong> populations, GLP-1R expression in both rodent and human kidneys is thought to be primarily confined to certain vascular smooth muscle cells. This review discusses recent advances in our understanding of the effects of GLP-1 medicines on the kidney with a focus on indirect and direct mechanisms of action.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 3","pages":"Article 101641"},"PeriodicalIF":4.6,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Despite associated risk of anemia and gastric cancer, screening for autoimmune atrophic gastritis (AAG) is underperformed in subjects with type 1 diabetes mellitus (T1DM). We measured the predictive value of serum gastrin as a biomarker of gastric atrophy in subjects with T1DM and parietal cell autoantibodies (PCA).
Subjects and Methods
PCA measurements were retrospectively retrieved in 1,425 consecutive subjects with T1DM between 2014 and 2018. Screening for AAG was conducted in PCA+ subjects by measuring blood counts, serum ferritin, vitamin B12 and gastrin; and by performing gastroduodenal fibroscopy, with fundic biopsies for histology and Helicobacter pylori. The performance of blood biomarkers of gastric atrophy was analyzed in comparison with the histopathological gold standard.
Results
PCA were found in 185/1,425 subjects (13 %). PCA positivity was associated with female sex, older age, longer T1DM duration, and co-occurrence of anti-GAD and anti-thyroperoxydase autoantibodies. Of the 185 PCA+ subjects, 122 (66 %) participated in screening. AAG was found in 69/122 (57 %) subjects and Helicobacter pylori infection in 20/122 (16 %). Compared to PCA+ subjects without gastric atrophy, those with gastric atrophy had more frequently iron deficiency (65 % vs. 18 %, P < 0.0001), and/or vitamin B12 deficiency (57 % vs. 7 %, P < 0.0001); 44/69 (64 %) presented a pre-tumoral lesion and 6 % a tumor. Using a cut-off of 1.2-fold above the upper normal limit, serum gastrin concentration displayed 91 % sensitivity and 82 % specificity at predicting gastric atrophy.
Conclusion
In subjects with T1DM and PCA, serum gastrin is a reliable biomarker of gastric atrophy that can be used to select subjects requiring gastroduodenal fibroscopy.
{"title":"Screening for autoimmune atrophic gastritis by serum gastrin measurement in subjects with type 1 diabetes","authors":"Aude Pacheco , Marc Diedisheim , Claire Goulvestre , Laure Alexandre-Heymann , Roberto Mallone , Danièle Dubois-Laforgue , Etienne Larger","doi":"10.1016/j.diabet.2025.101640","DOIUrl":"10.1016/j.diabet.2025.101640","url":null,"abstract":"<div><h3>Introduction</h3><div>Despite associated risk of anemia and gastric cancer, screening for autoimmune atrophic gastritis (AAG) is underperformed in subjects with type 1 diabetes mellitus (T1DM). We measured the predictive value of serum gastrin as a biomarker of gastric atrophy in subjects with T1DM and parietal cell autoantibodies (PCA).</div></div><div><h3>Subjects and Methods</h3><div>PCA measurements were retrospectively retrieved in 1,425 consecutive subjects with T1DM between 2014 and 2018. Screening for AAG was conducted in PCA+ subjects by measuring blood counts, serum ferritin, vitamin B12 and gastrin; and by performing gastroduodenal fibroscopy, with fundic biopsies for histology and <em>Helicobacter pylori</em>. The performance of blood biomarkers of gastric atrophy was analyzed in comparison with the histopathological gold standard.</div></div><div><h3>Results</h3><div>PCA were found in 185/1,425 subjects (13 %). PCA positivity was associated with female sex, older age, longer T1DM duration, and co-occurrence of anti-GAD and anti-thyroperoxydase autoantibodies. Of the 185 PCA+ subjects, 122 (66 %) participated in screening. AAG was found in 69/122 (57 %) subjects and <em>Helicobacter pylori</em> infection in 20/122 (16 %). Compared to PCA+ subjects without gastric atrophy, those with gastric atrophy had more frequently iron deficiency (65 % vs. 18 %, <em>P</em> < 0.0001), and/or vitamin B12 deficiency (57 % vs. 7 %, <em>P</em> < 0.0001); 44/69 (64 %) presented a pre-tumoral lesion and 6 % a tumor. Using a cut-off of 1.2-fold above the upper normal limit, serum gastrin concentration displayed 91 % sensitivity and 82 % specificity at predicting gastric atrophy.</div></div><div><h3>Conclusion</h3><div>In subjects with T1DM and PCA, serum gastrin is a reliable biomarker of gastric atrophy that can be used to select subjects requiring gastroduodenal fibroscopy.</div></div>","PeriodicalId":11334,"journal":{"name":"Diabetes & metabolism","volume":"51 3","pages":"Article 101640"},"PeriodicalIF":4.6,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143672166","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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