S. Li, S. Pan, N. Xiao, S. Jiang, G. G. Liu, and B. Lyu, “Prescription Medication Expenditures for Patients With Diabetes in the United States: 2012–2021,” Journal of Diabetes 17, no. 7 (2025): e70106, https://doi.org/10.1111/1753-0407.70106.
In the published version of the article, Figure 2 in the main text was incorrectly linked to Figure S4 (Supporting Information). The correct Figure 2 should correspond to the Graphical Abstract Image, as intended and originally submitted.
{"title":"Correction to “Prescription Medication Expenditures for Patients With Diabetes in the United States: 2012–2021”","authors":"","doi":"10.1111/1753-0407.70158","DOIUrl":"10.1111/1753-0407.70158","url":null,"abstract":"<p>S. Li, S. Pan, N. Xiao, S. Jiang, G. G. Liu, and B. Lyu, “Prescription Medication Expenditures for Patients With Diabetes in the United States: 2012–2021,” <i>Journal of Diabetes</i> 17, no. 7 (2025): e70106, https://doi.org/10.1111/1753-0407.70106.</p><p>In the published version of the article, Figure 2 in the main text was incorrectly linked to Figure S4 (Supporting Information). The correct Figure 2 should correspond to the Graphical Abstract Image, as intended and originally submitted.</p><p>We apologize for this error.</p>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243408","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}
Jia Ming Low, Abhishek Gupta, Rachel Toh, Su Lin Lim, Shiao-Yng Chan, Sanjay Swarup, Le Ye Lee
Background
Vertical transmission of microbes from a mother's gut to their offspring plays a crucial role in the genesis of the early life gut microbiome. Gestational Diabetes Mellitus (GDM) is the commonest metabolic disorder during pregnancy, which has adverse short- and long-term effects on both maternal and infant health. We aimed to capture the GDM-associated biosignatures in infants' gut microbiome from birth to the first 6 weeks of life.
Methods
53 GDM mother-infant dyads and 16 healthy mother-infant dyads were recruited. We performed targeted 16S rRNA gene amplicon sequencing on stool samples. Various statistical analyses were performed to understand the changes in the microbiome profile of infants and identify GDM-associated bacterial biomarkers in mothers and their transfer to infants.
Results
GDM altered the gut microbiome of pregnant women as compared to healthy counterparts (PERMANOVA, p.adjusted < 0.05), with predominance of bacterial members associated with insulin resistance, proinflammatory conditions, and other metabolic processes. Infants born to GDM mothers have distinctive early life microbiome (meconium and six weeks stools) compared to infants born to control mothers (PERMANOVA, p.adjusted < 0.05). We also identified the presence of various GDM-associated microbial signatures such as Blautia and Collinsella in both meconium and one-month-old stool samples of infants born to GDM mothers.
Conclusion
This study provides a better understanding of the impact of GDM on the seeding of a specific set of microbes during the early life colonization event in the infant gut that increases the risk of inflammatory and metabolic diseases in the future.
{"title":"Vertical Transmission of Gut Dysbiosis From Mothers With Gestational Diabetes to Infants","authors":"Jia Ming Low, Abhishek Gupta, Rachel Toh, Su Lin Lim, Shiao-Yng Chan, Sanjay Swarup, Le Ye Lee","doi":"10.1111/1753-0407.70148","DOIUrl":"https://doi.org/10.1111/1753-0407.70148","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Vertical transmission of microbes from a mother's gut to their offspring plays a crucial role in the genesis of the early life gut microbiome. Gestational Diabetes Mellitus (GDM) is the commonest metabolic disorder during pregnancy, which has adverse short- and long-term effects on both maternal and infant health. We aimed to capture the GDM-associated biosignatures in infants' gut microbiome from birth to the first 6 weeks of life.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>53 GDM mother-infant dyads and 16 healthy mother-infant dyads were recruited. We performed targeted 16S rRNA gene amplicon sequencing on stool samples. Various statistical analyses were performed to understand the changes in the microbiome profile of infants and identify GDM-associated bacterial biomarkers in mothers and their transfer to infants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>GDM altered the gut microbiome of pregnant women as compared to healthy counterparts (PERMANOVA, <i>p</i>.adjusted < 0.05), with predominance of bacterial members associated with insulin resistance, proinflammatory conditions, and other metabolic processes. Infants born to GDM mothers have distinctive early life microbiome (meconium and six weeks stools) compared to infants born to control mothers (PERMANOVA, <i>p</i>.adjusted < 0.05). We also identified the presence of various GDM-associated microbial signatures such as <i>Blautia</i> and <i>Collinsella</i> in both meconium and one-month-old stool samples of infants born to GDM mothers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study provides a better understanding of the impact of GDM on the seeding of a specific set of microbes during the early life colonization event in the infant gut that increases the risk of inflammatory and metabolic diseases in the future.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70148","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145196436","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}
Fasting blood glucose (FBG) reflects cardiometabolic health, but the long-term effects of childhood hypertension (HTN) on adult FBG are unclear.
Methods
Using data from the Bogalusa Heart Study, we examined the link between childhood HTN and FBG in early adulthood, adjusting for race, BMI, pulse rate, and blood pressure.
Results
Individuals with childhood HTN had higher FBG in early adulthood (mean difference 8.96 mg/dL) and a 4.16-fold higher risk of high FBG (≥ 126 mg/dL). The effect was stronger in African Americans, those with higher pulse rate, overweight individuals, or those with low diastolic BP.
Conclusions
Childhood HTN is linked to elevated FBG in early adulthood. Early management of hypertensive children, especially those at metabolic risk, may help prevent diabetes and cardiovascular disease later.
{"title":"History of Hypertension From Childhood and Fasting Blood Glucose Levels in Adulthood: The Bogalusa Study","authors":"Lingli Zhao, Jiahui Ouyang, Yewen Song, Hua Qu, Zhuye Gao","doi":"10.1111/1753-0407.70155","DOIUrl":"https://doi.org/10.1111/1753-0407.70155","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Fasting blood glucose (FBG) reflects cardiometabolic health, but the long-term effects of childhood hypertension (HTN) on adult FBG are unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using data from the Bogalusa Heart Study, we examined the link between childhood HTN and FBG in early adulthood, adjusting for race, BMI, pulse rate, and blood pressure.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Individuals with childhood HTN had higher FBG in early adulthood (mean difference 8.96 mg/dL) and a 4.16-fold higher risk of high FBG (≥ 126 mg/dL). The effect was stronger in African Americans, those with higher pulse rate, overweight individuals, or those with low diastolic BP.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Childhood HTN is linked to elevated FBG in early adulthood. Early management of hypertensive children, especially those at metabolic risk, may help prevent diabetes and cardiovascular disease later.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 10","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70155","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145196444","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}
This randomized controlled trial (RCT) was designed to evaluate the effects of sitagliptin on diabetic foot ulcers (DFUs).
Methods
This was a randomized, open-label clinical trial. The participants were assigned to either the control group, which received standard conventional therapy alone, or the sitagliptin treatment group, which received an oral administration of sitagliptin (100 mg once daily) in conjunction with standard conventional therapy. The primary endpoints were the ulcer healing rate and adverse reactions. The secondary endpoints included the time to ulcer healing, peripheral blood CD34+ endothelial progenitor cells (EPCs) count, serum levels of stromal cell-derived factor-1α (SDF-1α), and glycosylated hemoglobin A1c (HbA1c).
Results
A total of 62 subjects were enrolled in this trial, with 31 individuals assigned to each group. One participant from each group was lost to follow-up. Posttrial analysis revealed that, compared with the control group, the sitagliptin group demonstrated a significantly greater reduction in ulcer area and improved efficacy in terms of ulcer healing (p < 0.05). Although not statistically significant (p = 0.071), the sitagliptin group also tended to have a shorter ulcer healing time. Additionally, the sitagliptin group presented significantly greater numbers of CD34+ EPCs and higher SDF-1α levels compared to the control group (p < 0.05). No statistically significant difference in HbA1c levels was observed between the two groups (p > 0.05). No adverse events associated with sitagliptin treatment were reported.
Conclusions
The DPP-4 inhibitor sitagliptin may facilitate the healing of DFUs independent of its glucose-lowering effects, potentially by enhancing the mobilization of CD34 + EPCs in peripheral blood.
{"title":"Sitagliptin, a DPP-4 Inhibitor, Effectively Promotes the Healing of Diabetic Foot Ulcer: A Randomized Controlled Trial","authors":"Wei Gao, Dawei Chen, Hua He, Nenggang Jiang, Lihong Chen, Xingwu Ran","doi":"10.1111/1753-0407.70156","DOIUrl":"https://doi.org/10.1111/1753-0407.70156","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This randomized controlled trial (RCT) was designed to evaluate the effects of sitagliptin on diabetic foot ulcers (DFUs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This was a randomized, open-label clinical trial. The participants were assigned to either the control group, which received standard conventional therapy alone, or the sitagliptin treatment group, which received an oral administration of sitagliptin (100 mg once daily) in conjunction with standard conventional therapy. The primary endpoints were the ulcer healing rate and adverse reactions. The secondary endpoints included the time to ulcer healing, peripheral blood CD34+ endothelial progenitor cells (EPCs) count, serum levels of stromal cell-derived factor-1α (SDF-1α), and glycosylated hemoglobin A1c (HbA1c).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 62 subjects were enrolled in this trial, with 31 individuals assigned to each group. One participant from each group was lost to follow-up. Posttrial analysis revealed that, compared with the control group, the sitagliptin group demonstrated a significantly greater reduction in ulcer area and improved efficacy in terms of ulcer healing (<i>p</i> < 0.05). Although not statistically significant (<i>p</i> = 0.071), the sitagliptin group also tended to have a shorter ulcer healing time. Additionally, the sitagliptin group presented significantly greater numbers of CD34+ EPCs and higher SDF-1α levels compared to the control group (<i>p</i> < 0.05). No statistically significant difference in HbA1c levels was observed between the two groups (<i>p</i> > 0.05). No adverse events associated with sitagliptin treatment were reported.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The DPP-4 inhibitor sitagliptin may facilitate the healing of DFUs independent of its glucose-lowering effects, potentially by enhancing the mobilization of CD34 + EPCs in peripheral blood.</p>\u0000 \u0000 <p><b>Trial Registration:</b> Registration number: ChiCTR 2000029230, Approval date: 2020/01/19</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 9","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062792","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}
Diabetes is a global public health crisis, especially when it is accompanied by microvascular complications such as diabetic kidney disease (DKD). The purpose of this study was to explore the relationship between the combined lifestyle factors of diabetes patients and their joint effects with genetic risk and the risk of DKD.
Materials and Methods
We included individuals diagnosed with diabetes at baseline from UK Biobank. Their lifestyle information was collected through a baseline questionnaire. Favorable lifestyle scores were constructed based on 5 common lifestyle factors and categorized into three levels. Genetic susceptibility to CKD was estimated by polygenic risk scores and further categorized into high, and low genetic risk categories. Cox proportional hazards regression model was used to estimate the hazard ratios (HR) and 95% confidence interval (CI) for their associations.
Results
By the end of follow-up, 1335 of 11 981 diabetes patients progressed to diabetes nephropathy. The COX regression results indicate that BMI ≥ 25 mg/m2 and current or past smoking were risk factors for DKD, while alcohol consumption and moderate to high-intensity pysical exercise were protective factors. High genetic risk is significantly associated with increased risk of DKD (HR1.29, 95% CI 1.13–1.47, p < 0.001), while a favorable lifestyle had a protective effect (HR0.47, 95% CI 0.37–0.59, p < 0.001). Interaction analysis shows that there was neither additive nor multiplicative interaction between genetic risk and lifestyle.
Conclusions
Lifestyle factors and genetics are independently associated with susceptibility to incident DKD. A healthy lifestyle may attenuate elevated DKD risks due to genetic vulnerability.
目的：糖尿病是一个全球性的公共卫生危机，特别是当它伴有微血管并发症，如糖尿病肾病（DKD）时。本研究旨在探讨糖尿病患者的综合生活方式因素及其与遗传风险和DKD风险的共同作用之间的关系。材料和方法：我们纳入了来自UK Biobank的基线诊断为糖尿病的个体。他们的生活方式信息是通过基线问卷收集的。根据5个常见的生活方式因素构建良好的生活方式评分，分为3个等级。通过多基因风险评分来评估CKD的遗传易感性，并进一步分为高遗传风险和低遗传风险类别。采用Cox比例风险回归模型估计其相关性的风险比（HR）和95%置信区间（CI）。结果：随访结束时，11,981例糖尿病患者中有1335例进展为糖尿病肾病。COX回归结果显示，BMI≥25 mg/m2和当前或过去吸烟是DKD的危险因素，而饮酒和中高强度体育锻炼是DKD的保护因素。高遗传风险与DKD风险增加显著相关（HR1.29, 95% CI 1.13-1.47, p）。结论：生活方式因素和遗传与DKD易感性独立相关。健康的生活方式可以降低由于遗传易感性而增加的DKD风险。
{"title":"The Contribution of Genetic Risk and Lifestyle Factors in the Progression of Diabetes to Diabetic Kidney Disease: A Prospective Cohort Study","authors":"Yujiao Wang, Chunyang Li, Nongbu Cili, Jing Chen, Huazhen Yang, Ping Fu, Xiaoxi Zeng","doi":"10.1111/1753-0407.70141","DOIUrl":"10.1111/1753-0407.70141","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Diabetes is a global public health crisis, especially when it is accompanied by microvascular complications such as diabetic kidney disease (DKD). The purpose of this study was to explore the relationship between the combined lifestyle factors of diabetes patients and their joint effects with genetic risk and the risk of DKD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>We included individuals diagnosed with diabetes at baseline from UK Biobank. Their lifestyle information was collected through a baseline questionnaire. Favorable lifestyle scores were constructed based on 5 common lifestyle factors and categorized into three levels. Genetic susceptibility to CKD was estimated by polygenic risk scores and further categorized into high, and low genetic risk categories. Cox proportional hazards regression model was used to estimate the hazard ratios (HR) and 95% confidence interval (CI) for their associations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>By the end of follow-up, 1335 of 11 981 diabetes patients progressed to diabetes nephropathy. The COX regression results indicate that BMI ≥ 25 mg/m<sup>2</sup> and current or past smoking were risk factors for DKD, while alcohol consumption and moderate to high-intensity pysical exercise were protective factors. High genetic risk is significantly associated with increased risk of DKD (HR1.29, 95% CI 1.13–1.47, <i>p</i> < 0.001), while a favorable lifestyle had a protective effect (HR0.47, 95% CI 0.37–0.59, <i>p</i> < 0.001). Interaction analysis shows that there was neither additive nor multiplicative interaction between genetic risk and lifestyle.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Lifestyle factors and genetics are independently associated with susceptibility to incident DKD. A healthy lifestyle may attenuate elevated DKD risks due to genetic vulnerability.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 9","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032341","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}
<p>The major determinants of the development of chronic kidney disease (CKD) in people with diabetes are hyperglycemia, hypertension, genetic susceptibility, dyslipidemia, and inflammation. By better understanding these factors, we can modify the risk of kidney damage and subsequent complications among people with diabetes. Elevation in glucose levels leads to both metabolic and hemodynamic changes, including glomerular hyperfiltration, podocyte injury, and progressive albuminuria, while hypertension accelerates glomerular damage [<span>1</span>]. Genetic predisposition, along with lifestyle factors such as obesity and smoking, further increases the risk. Dyslipidemia and oxidative stress contribute to endothelial dysfunction and tubulointerstitial injury [<span>2</span>], and inflammation [<span>3</span>] and activation of fibrotic pathways play important roles in disease progression [<span>4, 5</span>].</p><p>CKD is defined operationally by estimated glomerular filtrate rate (eGFR) < 60 mL/min and urine albumin/creatinine ratio (UACR) ≥ 30 mg/g present for 90 days or longer. Diabetes is responsible for roughly one-quarter to one-half of all CKD cases, with the proportion varying by region, population demographics, and stage of kidney disease [<span>6-8</span>]. This underscores the critical importance of diabetes prevention and optimal management to reduce the global burden of CKD. Albuminuria with normal renal function and/or an eGFR < 60 mL/min is associated with considerable cardiovascular mortality and heart failure risk. This has been underappreciated compared to the risk of progression of CKD and ESKD. In diabetic CKD, the risk of cardiovascular death is twice as great with eGFR < 60 mL/min and four times as great with eGFR < 45 mL/min, compared to normal renal function [<span>9</span>]. Compared to no albuminuria, mortality and heart failure admissions are four- and five-fold more likely in the presence of albuminuria, even when the eGFR is normal [<span>10, 11</span>].</p><p>Pharmacologic therapy is the cornerstone of treatment of diabetic CKD, with improvement in outcome seen with Renin-Angiotensin-Aldosterone system (RAAS) blockade, including mineralocorticoid inhibitors (MRA), sodium glucose transporter (SGLT) 2 inhibitors, and glucagon-like peptide (GLP)-1 receptor agonists (RA); significant therapeutic benefits also have been shown with aggressive therapy of comorbidities (hypertension, obesity and dyslipidemia) [<span>12</span>]. However, lifestyle modifications (diet/weight management, physical activity, smoking) and genetic risk have not received as much attention in clinical practice [<span>13</span>]. In a Dutch observational study, only 2% of patients adhered to all recommended lifestyle recommendations [<span>14</span>].</p><p>Three publications in the current Journal of Diabetes evaluate the aspects of the effects of lifestyle, social factors, genetic risks, and comorbidities as risk factors for the progression
{"title":"Diabetic Kidney Disease Update","authors":"Christian Mende, Zachary Bloomgarden","doi":"10.1111/1753-0407.70150","DOIUrl":"https://doi.org/10.1111/1753-0407.70150","url":null,"abstract":"<p>The major determinants of the development of chronic kidney disease (CKD) in people with diabetes are hyperglycemia, hypertension, genetic susceptibility, dyslipidemia, and inflammation. By better understanding these factors, we can modify the risk of kidney damage and subsequent complications among people with diabetes. Elevation in glucose levels leads to both metabolic and hemodynamic changes, including glomerular hyperfiltration, podocyte injury, and progressive albuminuria, while hypertension accelerates glomerular damage [<span>1</span>]. Genetic predisposition, along with lifestyle factors such as obesity and smoking, further increases the risk. Dyslipidemia and oxidative stress contribute to endothelial dysfunction and tubulointerstitial injury [<span>2</span>], and inflammation [<span>3</span>] and activation of fibrotic pathways play important roles in disease progression [<span>4, 5</span>].</p><p>CKD is defined operationally by estimated glomerular filtrate rate (eGFR) < 60 mL/min and urine albumin/creatinine ratio (UACR) ≥ 30 mg/g present for 90 days or longer. Diabetes is responsible for roughly one-quarter to one-half of all CKD cases, with the proportion varying by region, population demographics, and stage of kidney disease [<span>6-8</span>]. This underscores the critical importance of diabetes prevention and optimal management to reduce the global burden of CKD. Albuminuria with normal renal function and/or an eGFR < 60 mL/min is associated with considerable cardiovascular mortality and heart failure risk. This has been underappreciated compared to the risk of progression of CKD and ESKD. In diabetic CKD, the risk of cardiovascular death is twice as great with eGFR < 60 mL/min and four times as great with eGFR < 45 mL/min, compared to normal renal function [<span>9</span>]. Compared to no albuminuria, mortality and heart failure admissions are four- and five-fold more likely in the presence of albuminuria, even when the eGFR is normal [<span>10, 11</span>].</p><p>Pharmacologic therapy is the cornerstone of treatment of diabetic CKD, with improvement in outcome seen with Renin-Angiotensin-Aldosterone system (RAAS) blockade, including mineralocorticoid inhibitors (MRA), sodium glucose transporter (SGLT) 2 inhibitors, and glucagon-like peptide (GLP)-1 receptor agonists (RA); significant therapeutic benefits also have been shown with aggressive therapy of comorbidities (hypertension, obesity and dyslipidemia) [<span>12</span>]. However, lifestyle modifications (diet/weight management, physical activity, smoking) and genetic risk have not received as much attention in clinical practice [<span>13</span>]. In a Dutch observational study, only 2% of patients adhered to all recommended lifestyle recommendations [<span>14</span>].</p><p>Three publications in the current Journal of Diabetes evaluate the aspects of the effects of lifestyle, social factors, genetic risks, and comorbidities as risk factors for the progression ","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 9","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144990708","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 increased risk of ischemic events in diabetes, the optimal anti-thrombotic strategy for secondary prevention has not been defined. We aimed to assess the efficacy and safety of optimal antiplatelet agents such as indobufen-based dual antiplatelet therapy (DAPT) in patients with diabetes after coronary stenting.
Methods
OPTION trial was a randomized, open-label, noninferiority, and multicentric study in China. Enrolled subjects were randomized 1:1 to indobufen-based DAPT or aspirin-based DAPT. This post hoc analysis from OPTION trial was performed by the presence of diabetes. The primary endpoint was a 1-year composite of cardiovascular death, nonfatal myocardial infarction, ischemic stroke, definite or probable stent thrombosis, or Bleeding Academic Research Consortium (BARC) criteria type 2, 3, or 5 bleeding.
Results
Of 4551 OPTION patients, the primary endpoint occurred in 93/1570 patients with diabetes (5.92%), as compared to 148/2981 without diabetes (4.96%) (HR: 0.72, 95% CI: 0.47–1.08, and HR: 0.73, 95% CI: 0.53–1.01, respectively), without significant interaction between diabetes status and treatment effect (Pinteraction = 0.935). The secondary efficacy endpoint was comparable between patients with (HR: 1.31, 95% CI: 0.60–2.84) and without diabetes (HR: 0.95, 95% CI: 0.51–1.76) (Pinteraction = 0.526). Similarly, both subgroups derived similar benefits for the safety endpoint (HR, 0.56; 95% CI, 0.34–0.92 for subjects with diabetes vs. HR, 0.66; 95% CI, 0.45–0.98 for those without diabetes; Pinteraction = 0.609).
Conclusions
In patients receiving DES implantation, indobufen-based DAPT might be considered as a reasonable alternative to aspirin-based DAPT in the secondary prevention for those with diabetes, especially in patients at high bleeding risk.
{"title":"Indobufen Versus Aspirin Plus Clopidogrel in Patients After Coronary Stenting in Patients With Diabetes: A Post Hoc Analysis of the OPTION Trial","authors":"Shujing Wu, Huajie Xu, Lili Xu, Huanyi Zhang, Kang Cheng, Xiaoyan Wang, Manhua Chen, Guangping Li, Jiangnan Huang, Jun Lan, Guanghe Wei, Xin Zhao, Zhiyong Qi, Juying Qian, Hongyi Wu, Junbo Ge, the OPTION investigators","doi":"10.1111/1753-0407.70152","DOIUrl":"https://doi.org/10.1111/1753-0407.70152","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Despite increased risk of ischemic events in diabetes, the optimal anti-thrombotic strategy for secondary prevention has not been defined. We aimed to assess the efficacy and safety of optimal antiplatelet agents such as indobufen-based dual antiplatelet therapy (DAPT) in patients with diabetes after coronary stenting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>OPTION trial was a randomized, open-label, noninferiority, and multicentric study in China. Enrolled subjects were randomized 1:1 to indobufen-based DAPT or aspirin-based DAPT. This post hoc analysis from OPTION trial was performed by the presence of diabetes. The primary endpoint was a 1-year composite of cardiovascular death, nonfatal myocardial infarction, ischemic stroke, definite or probable stent thrombosis, or Bleeding Academic Research Consortium (BARC) criteria type 2, 3, or 5 bleeding.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 4551 OPTION patients, the primary endpoint occurred in 93/1570 patients with diabetes (5.92%), as compared to 148/2981 without diabetes (4.96%) (HR: 0.72, 95% CI: 0.47–1.08, and HR: 0.73, 95% CI: 0.53–1.01, respectively), without significant interaction between diabetes status and treatment effect (<i>P</i><sub>interaction</sub> = 0.935). The secondary efficacy endpoint was comparable between patients with (HR: 1.31, 95% CI: 0.60–2.84) and without diabetes (HR: 0.95, 95% CI: 0.51–1.76) (<i>P</i><sub>interaction</sub> = 0.526). Similarly, both subgroups derived similar benefits for the safety endpoint (HR, 0.56; 95% CI, 0.34–0.92 for subjects with diabetes vs. HR, 0.66; 95% CI, 0.45–0.98 for those without diabetes; <i>P</i><sub>interaction</sub> = 0.609).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In patients receiving DES implantation, indobufen-based DAPT might be considered as a reasonable alternative to aspirin-based DAPT in the secondary prevention for those with diabetes, especially in patients at high bleeding risk.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 9","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70152","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144990709","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}
Limited empirical evidence exists on the link between exposure to various stressful life events (SLEs) and the heightened risk of Diabetes Mellitus (DM) within the mainland Chinese population.
Methods
We conducted this prospective cohort study with 455,464 participants from the China Kadoorie Biobank (CKB); we examined associations between SLEs exposures and DM outcomes. We employed multivariable Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for potential confounders.
Results
Over a median follow-up of 10.1 years, 14,218 DM cases were identified. A dose–response relationship was observed between the number of SLEs, personal-related events, and the risk of DM. The higher the number of SLEs experienced, the higher the risk of developing diabetes (HR = 1.06, 95% CI = 1.01–1.12); individuals who experienced personal-related events had a higher risk of developing DM (HR = 1.17, 95% CI = 1.01–1.36), and those who experienced marital separation/divorce had a 53% increased risk of DM (HR = 1.53, 95% CI = 1.12–2.09). Subgroup analyses revealed effect modifications based on birth cohort, sex, and area.
Conclusion
By exploring the association of multiple SLEs with the development of DM, we identified marital separation/divorce as a driver of increased DM risk.
背景在中国大陆人群中，暴露于各种应激性生活事件（SLEs）与糖尿病（DM）风险升高之间的联系存在有限的经验证据。方法：我们对来自中国嘉道理生物库（CKB）的455,464名参与者进行了前瞻性队列研究；我们研究了SLEs暴露与糖尿病结局之间的关系。我们采用多变量Cox比例风险模型来估计风险比（hr）和95%置信区间（ci），并对潜在混杂因素进行调整。结果在10.1年的中位随访中，共发现14218例糖尿病病例。SLEs次数、个人相关事件与糖尿病风险之间存在剂量-反应关系。经历SLEs次数越多，发生糖尿病的风险越高（HR = 1.06, 95% CI = 1.01-1.12）；经历过个人相关事件的人患糖尿病的风险更高（HR = 1.17, 95% CI = 1.01-1.36），经历过婚姻分居/离婚的人患糖尿病的风险增加53% （HR = 1.53, 95% CI = 1.12-2.09）。亚组分析显示基于出生队列、性别和地区的效果改变。结论：通过探索多重SLEs与糖尿病发展的关系，我们确定婚姻分居/离婚是糖尿病风险增加的驱动因素。
{"title":"Associations of Stressful Life Events With Diabetes Incidence in China: Insights From the China Kadoorie Biobank","authors":"Jing Qian, Huiying Cheng, Xuening Dai, Dianjianyi Sun, Pei Pei, Meng Wang, Yingjun Li","doi":"10.1111/1753-0407.70149","DOIUrl":"https://doi.org/10.1111/1753-0407.70149","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Limited empirical evidence exists on the link between exposure to various stressful life events (SLEs) and the heightened risk of Diabetes Mellitus (DM) within the mainland Chinese population.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted this prospective cohort study with 455,464 participants from the China Kadoorie Biobank (CKB); we examined associations between SLEs exposures and DM outcomes. We employed multivariable Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusting for potential confounders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Over a median follow-up of 10.1 years, 14,218 DM cases were identified. A dose–response relationship was observed between the number of SLEs, personal-related events, and the risk of DM. The higher the number of SLEs experienced, the higher the risk of developing diabetes (HR = 1.06, 95% CI = 1.01–1.12); individuals who experienced personal-related events had a higher risk of developing DM (HR = 1.17, 95% CI = 1.01–1.36), and those who experienced marital separation/divorce had a 53% increased risk of DM (HR = 1.53, 95% CI = 1.12–2.09). Subgroup analyses revealed effect modifications based on birth cohort, sex, and area.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>By exploring the association of multiple SLEs with the development of DM, we identified marital separation/divorce as a driver of increased DM risk.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 9","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70149","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144923689","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}
This meta-analysis aims to assess the association between exposure to glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and the incidence of suicidal behavior in patients with type 2 diabetes mellitus (T2DM)/obesity.
Methods
A comprehensive search of electronic databases, including PubMed, Web of Science, the Cochrane Library, and ClinicalTrials.gov, was conducted from the inception of the databases. The risk ratio (RR) and 95% confidence intervals (95% CI) were calculated.
Results
This meta-analysis included data from 25 randomized controlled trials (RCTs). The results indicated no significant difference in the incidence of suicidal behavior between the GLP-1 RA exposure group and the control group (RR = 0.84, 95% CI: 0.54–1.32, p = 0.46, I2 = 0%). Subgroup analysis showed no significant differences in the incidence of suicidal behavior among participants with T2DM (RR = 0.74), obesity (RR = 1.07), adolescents (RR = 0.91), and adults (RR = 0.84). Additionally, no significant differences were observed between the two groups in any type of suicidal behavior, including suicidal ideation (RR = 1.04), suicide attempts (RR = 0.68), depression-related suicides (RR = 0.65), and completed suicides (RR = 1.06). There were also no significant differences between the groups for any type of GLP-1 RA, including dulaglutide (RR = 0.46), exenatide (RR = 0.98), semaglutide (RR = 0.82), lixisenatide (RR = 1.25), and liraglutide (RR = 0.92). No significant differences were observed between the exposure group and control group according to different comparators, including placebo (RR = 0.91) and others (RR = 1.08). All subgroup analyses showed p-values greater than 0.05 (two-sided tests) and I2 values of 0%.
Conclusion
Our findings suggest that there is no significant association between GLP-1 RA exposure and suicidal behaviors in patients with T2DM or obesity.
{"title":"Impact of GLP-1 Receptor Agonists on Suicide Behavior: A Meta-Analysis Based on Randomized Controlled Trials","authors":"Jingqi Chen, Qiufeng Zhang, Qingping Wu, Xiaoming Zhang, Zhiyi Xiang, Sidong Zhu, Tianfu Dai, Yuexiu Si","doi":"10.1111/1753-0407.70151","DOIUrl":"https://doi.org/10.1111/1753-0407.70151","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This meta-analysis aims to assess the association between exposure to glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and the incidence of suicidal behavior in patients with type 2 diabetes mellitus (T2DM)/obesity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive search of electronic databases, including PubMed, Web of Science, the Cochrane Library, and ClinicalTrials.gov, was conducted from the inception of the databases. The risk ratio (RR) and 95% confidence intervals (95% CI) were calculated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>This meta-analysis included data from 25 randomized controlled trials (RCTs). The results indicated no significant difference in the incidence of suicidal behavior between the GLP-1 RA exposure group and the control group (RR = 0.84, 95% CI: 0.54–1.32, <i>p</i> = 0.46, <i>I</i><sup>2</sup> = 0%). Subgroup analysis showed no significant differences in the incidence of suicidal behavior among participants with T2DM (RR = 0.74), obesity (RR = 1.07), adolescents (RR = 0.91), and adults (RR = 0.84). Additionally, no significant differences were observed between the two groups in any type of suicidal behavior, including suicidal ideation (RR = 1.04), suicide attempts (RR = 0.68), depression-related suicides (RR = 0.65), and completed suicides (RR = 1.06). There were also no significant differences between the groups for any type of GLP-1 RA, including dulaglutide (RR = 0.46), exenatide (RR = 0.98), semaglutide (RR = 0.82), lixisenatide (RR = 1.25), and liraglutide (RR = 0.92). No significant differences were observed between the exposure group and control group according to different comparators, including placebo (RR = 0.91) and others (RR = 1.08). All subgroup analyses showed <i>p</i>-values greater than 0.05 (two-sided tests) and <i>I</i><sup>2</sup> values of 0%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our findings suggest that there is no significant association between GLP-1 RA exposure and suicidal behaviors in patients with T2DM or obesity.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 9","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70151","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144923805","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}
Lei Xi, Juan Shi, Ying Peng, Yifei Zhang, Yanan Cao, Weiqing Wang
We thank the authors for their insightful comments and for recognizing that our manuscript provides valuable details about behavioral and genetic factors affecting the risk of obesity in people with type 2 diabetes (T2D) [1].
Firstly, as mentioned in our article, there may be recall bias based on patient self-reported sleep duration, and objectively measuring habitual sleep duration using actigraphy can provide more reliable data. However, considering its simplicity, practicality, and correlation with instrument measurement results, patients' self-reported sleep duration is still internationally recognized and widely used in population-based studies [2, 3].
Secondly, the relationship between sleep, diabetes and obesity is really complex and challenging. As mentioned by the authors, most exploratory experiments on sleep are temporary, especially for sleep deprivation. There are interactions among sleep, diabetes and obesity that impact cardiovascular and metabolic health, just like the intertwined trio. To avoid the potential impact of sleep related diseases, we excluded patients who reported implausible values of sleep duration (i.e., < 3 or > 12 h/night), use of sleeping aids, or psychiatric medications at baseline. It should be pointed out that the above efforts cannot completely eliminate the potential impact of sleep disorders on our study results, and how to reduce their potential effects is also one of the key considerations in our future research. The Pittsburgh Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS) are indeed effective tools.
As we mentioned in the article, we acknowledge that “although we have adjusted for several covariates, there are potential confounders that could influence the results, such as dietary habits, physical activity, socioeconomic biases, and glucose-lowering medications, which we did not include in this study, and further research is needed to strengthen our understanding of these complex associations”, when it comes to both clinical and genetic analysis. In addition, a more complex and precise polygenic risk score (PRS) model for body mass index (BMI) is also under consideration.
In conclusion, we thank the authors for the wise and valuable comments and suggestions. We hope these clarifications address the issues raised and we intend to use more complex and appropriate models to explore their associations in future research.
{"title":"Response to Commentary on “Sleep Phenotypes, Genetic Susceptibility, and Risk of Obesity in Patients With Type 2 Diabetes: A National Prospective Cohort Study”","authors":"Lei Xi, Juan Shi, Ying Peng, Yifei Zhang, Yanan Cao, Weiqing Wang","doi":"10.1111/1753-0407.70145","DOIUrl":"https://doi.org/10.1111/1753-0407.70145","url":null,"abstract":"<p>We thank the authors for their insightful comments and for recognizing that our manuscript provides valuable details about behavioral and genetic factors affecting the risk of obesity in people with type 2 diabetes (T2D) [<span>1</span>].</p><p>Firstly, as mentioned in our article, there may be recall bias based on patient self-reported sleep duration, and objectively measuring habitual sleep duration using actigraphy can provide more reliable data. However, considering its simplicity, practicality, and correlation with instrument measurement results, patients' self-reported sleep duration is still internationally recognized and widely used in population-based studies [<span>2, 3</span>].</p><p>Secondly, the relationship between sleep, diabetes and obesity is really complex and challenging. As mentioned by the authors, most exploratory experiments on sleep are temporary, especially for sleep deprivation. There are interactions among sleep, diabetes and obesity that impact cardiovascular and metabolic health, just like the intertwined trio. To avoid the potential impact of sleep related diseases, we excluded patients who reported implausible values of sleep duration (i.e., < 3 or > 12 h/night), use of sleeping aids, or psychiatric medications at baseline. It should be pointed out that the above efforts cannot completely eliminate the potential impact of sleep disorders on our study results, and how to reduce their potential effects is also one of the key considerations in our future research. The Pittsburgh Sleep Quality Index (PSQI) and the Epworth Sleepiness Scale (ESS) are indeed effective tools.</p><p>As we mentioned in the article, we acknowledge that “although we have adjusted for several covariates, there are potential confounders that could influence the results, such as dietary habits, physical activity, socioeconomic biases, and glucose-lowering medications, which we did not include in this study, and further research is needed to strengthen our understanding of these complex associations”, when it comes to both clinical and genetic analysis. In addition, a more complex and precise polygenic risk score (PRS) model for body mass index (BMI) is also under consideration.</p><p>In conclusion, we thank the authors for the wise and valuable comments and suggestions. We hope these clarifications address the issues raised and we intend to use more complex and appropriate models to explore their associations in future research.</p><p>The authors declare no conflicts of interest.</p>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70145","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144891692","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}
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