Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder where the immune system targets and destroys insulin-producing β-cells in the pancreas. It generally emerges during childhood or adolescence, but individuals of any age can be affected. In contrast to Type 2 diabetes mellitus (T2DM) which is often associated with lifestyle factors, T1DM cannot be prevented and necessitates lifelong management. Currently, there is no definitive cure for T1DM, and patients rely on continuous insulin injections for their entire lives. Ongoing developments in insulin treatment, such as insulin pumps, continuous glucose monitoring, and hybrid closed-loop systems, offer promising alternatives. Despite advancements in intensive glycemic control that have reduced the occurrence of microvascular and macrovascular complications, a significant number of T1DM patients still these issues. Extensive research efforts are crucial to achieve early detection, prevent the loss of β-cells, and devise improved treatment strategies to enhance the quality of life and prognosis for those affected. This review explores the most noteworthy and recent advancements in the field of T1DM.
{"title":"A Comprehensive Review of Novel Advances in Type 1 Diabetes Mellitus","authors":"Yazdan Ebrahimpour, Sahbasadat Khatami, Mahsa Saffar, Alireza Fereidouni, Zahra Biniaz, Nafiseh Erfanian, Mohammad Fereidouni","doi":"10.1111/1753-0407.70120","DOIUrl":"https://doi.org/10.1111/1753-0407.70120","url":null,"abstract":"<p>Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder where the immune system targets and destroys insulin-producing β-cells in the pancreas. It generally emerges during childhood or adolescence, but individuals of any age can be affected. In contrast to Type 2 diabetes mellitus (T2DM) which is often associated with lifestyle factors, T1DM cannot be prevented and necessitates lifelong management. Currently, there is no definitive cure for T1DM, and patients rely on continuous insulin injections for their entire lives. Ongoing developments in insulin treatment, such as insulin pumps, continuous glucose monitoring, and hybrid closed-loop systems, offer promising alternatives. Despite advancements in intensive glycemic control that have reduced the occurrence of microvascular and macrovascular complications, a significant number of T1DM patients still these issues. Extensive research efforts are crucial to achieve early detection, prevent the loss of β-cells, and devise improved treatment strategies to enhance the quality of life and prognosis for those affected. This review explores the most noteworthy and recent advancements in the field of T1DM.</p>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70120","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782283","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}
Periodontal disease is a prevalent and chronic inflammatory condition increasingly recognized for its systemic implications beyond oral health. While traditionally confined to dentistry, recent evidence reveals strong associations between periodontitis and chronic systemic conditions such as cardiovascular disease, diabetes mellitus, rheumatoid arthritis, inflammatory bowel disease, Alzheimer's disease, and various cancers. Mechanistic studies have identified plausible biological pathways, including systemic dissemination of periodontal pathogens and immune mediators, which can exacerbate distant organ inflammation and dysfunction. Experimental models highlight how oral bacteria influence immune responses, disrupt gut and vascular homeostasis, and contribute to oncogenesis and autoimmunity. Notably, bidirectional relationships, such as those between periodontitis and diabetes, underscore the need for integrated care approaches. Effective periodontal therapy has demonstrated systemic benefits, including improved glycemic control and reduced inflammation. Given the mounting evidence, periodontal disease should be approached as a critical component of systemic health, necessitating interdisciplinary collaboration among healthcare providers to optimize patient outcomes and public health.
{"title":"Periodontal Disease: A Contributing Factor to Adverse Outcome in Diabetes","authors":"Edgard El Chaar","doi":"10.1111/1753-0407.70136","DOIUrl":"https://doi.org/10.1111/1753-0407.70136","url":null,"abstract":"<p>Periodontal disease is a prevalent and chronic inflammatory condition increasingly recognized for its systemic implications beyond oral health. While traditionally confined to dentistry, recent evidence reveals strong associations between periodontitis and chronic systemic conditions such as cardiovascular disease, diabetes mellitus, rheumatoid arthritis, inflammatory bowel disease, Alzheimer's disease, and various cancers. Mechanistic studies have identified plausible biological pathways, including systemic dissemination of periodontal pathogens and immune mediators, which can exacerbate distant organ inflammation and dysfunction. Experimental models highlight how oral bacteria influence immune responses, disrupt gut and vascular homeostasis, and contribute to oncogenesis and autoimmunity. Notably, bidirectional relationships, such as those between periodontitis and diabetes, underscore the need for integrated care approaches. Effective periodontal therapy has demonstrated systemic benefits, including improved glycemic control and reduced inflammation. Given the mounting evidence, periodontal disease should be approached as a critical component of systemic health, necessitating interdisciplinary collaboration among healthcare providers to optimize patient outcomes and public health.</p>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767694","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}
Lijuan Xu, Liehua Liu, Zhiwei Xie, Zhimin Huang, Hai Li, Juan Liu, Xiaoying He, Wanping Deng, Yanbing Li
Background
Early short-term intensive insulin therapy may induce sustained glycemic remission in type 2 diabetes. However, patients' responses vary greatly. Exploring key factors to improve glycemic control and predict the probability of remission precisely is meaningful for future treatment.
Methods
Patients with newly diagnosed type 2 diabetes receiving 2–3 weeks of intensive insulin therapy were followed up for at least 1 year in three randomized clinical trials. Data of theirs were extracted with the same inclusion criteria and divided into training and validation sets. A nomogram was constructed in the training set and tested in the internal validation set.
Results
Among 302 patients with transient intensive insulin therapy, 162 (53.64%) patients achieved the 1-year glycemic remission. Severe hyperglycemia at baseline did not impede future remission, as the remission rate was 60.70% in those with HbA1c greater than 13%. Three parameters were identified as predictive factors in the nomogram: fasting glucose after short-term insulin treatment, mean glucose during insulin therapy, and postprandial glucose/fasting glucose ratio at baseline. The odds ratios were 0.06 (95% CI, 0.02–0.25), 0.41 (0.18–0.93) and 6.55 (1.39–30.89), respectively. Incorporating these factors, the nomogram achieved an accuracy of 81.50%.
Conclusion
Short-term intensive insulin therapy assists patients with newly diagnosed type 2 diabetes and significant hyperglycemia to achieve glycemic remission. A rigorous control of glucose during insulin treatment favors future remission. We construct a nomogram to predict sustained glycemic remission, which may help determine whether subsequent medication is needed and thus reduce both overtreatment and therapeutic inertia.
{"title":"Construction and Implications of Nomogram for Predicting Sustained Glycemic Remission After Short-Term Intensive Insulin Therapy in Newly Diagnosed Type 2 Diabetes","authors":"Lijuan Xu, Liehua Liu, Zhiwei Xie, Zhimin Huang, Hai Li, Juan Liu, Xiaoying He, Wanping Deng, Yanbing Li","doi":"10.1111/1753-0407.70135","DOIUrl":"https://doi.org/10.1111/1753-0407.70135","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Early short-term intensive insulin therapy may induce sustained glycemic remission in type 2 diabetes. However, patients' responses vary greatly. Exploring key factors to improve glycemic control and predict the probability of remission precisely is meaningful for future treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Patients with newly diagnosed type 2 diabetes receiving 2–3 weeks of intensive insulin therapy were followed up for at least 1 year in three randomized clinical trials. Data of theirs were extracted with the same inclusion criteria and divided into training and validation sets. A nomogram was constructed in the training set and tested in the internal validation set.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 302 patients with transient intensive insulin therapy, 162 (53.64%) patients achieved the 1-year glycemic remission. Severe hyperglycemia at baseline did not impede future remission, as the remission rate was 60.70% in those with HbA1c greater than 13%. Three parameters were identified as predictive factors in the nomogram: fasting glucose after short-term insulin treatment, mean glucose during insulin therapy, and postprandial glucose/fasting glucose ratio at baseline. The odds ratios were 0.06 (95% CI, 0.02–0.25), 0.41 (0.18–0.93) and 6.55 (1.39–30.89), respectively. Incorporating these factors, the nomogram achieved an accuracy of 81.50%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Short-term intensive insulin therapy assists patients with newly diagnosed type 2 diabetes and significant hyperglycemia to achieve glycemic remission. A rigorous control of glucose during insulin treatment favors future remission. We construct a nomogram to predict sustained glycemic remission, which may help determine whether subsequent medication is needed and thus reduce both overtreatment and therapeutic inertia.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144751424","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}
Lin Ding, Xiaojing Lin, Peipei Pan, Yan Li, Wei Chen, Liying He, Yunsheng Xu, Hsun-Ming Chang, Haiyan Yang, Guiquan Wang, Liangshan Mu
Objectives
Whether diverse metabolic statuses within a similar body mass index (BMI) category associate with different in vitro fertilization (IVF) outcomes.
Design
A retrospective cohort study.
Setting
Wenzhou, Zhengjiang Province, China.
Population
This retrospective cohort study prescreened 16 458 women who underwent their first IVF and fresh embryo transfer cycle between January 2010 and December 2021.
Methods
Metabolic status was assessed using the National Cholesterol Education Program–Adult Treatment Panel III criteria. Patients were then categorized into six groups: metabolically healthy normal weight, metabolically unhealthy normal weight, metabolically healthy overweight, metabolically unhealthy overweight, metabolically healthy obese, and metabolically unhealthy obese.
Main Outcome Measures
The primary outcome was live birth rate.
Results
Regarding live birth, rates in normal weight women were initially lower for metabolically unhealthy normal weight versus metabolically healthy normal weight (44.6% vs. 48.6%), but this was not significant after multivariate adjustment. In obese women, live birth rates were similar between metabolically unhealthy obese and metabolically healthy obese (41.5% vs. 43.9%), with no adjusted difference. For secondary outcomes, metabolically unhealthy normal weight patients had lower biochemical pregnancy rates than metabolically healthy normal weight (OR: 0.86, 95% CI: 0.76–0.98); high blood pressure was a significant risk factor for this outcome in metabolically unhealthy normal weight (OR: 0.84, 95% CI: 0.72–0.98).
Conclusion
Our findings indicated that different cardio-metabolic risk factors but a similar BMI category may have limited adverse effects on live birth rate.
{"title":"Does Metabolic Status Associate With IVF Outcomes in Women Within Similar Body Mass Index Category: Evidence From a Large Cohort Study","authors":"Lin Ding, Xiaojing Lin, Peipei Pan, Yan Li, Wei Chen, Liying He, Yunsheng Xu, Hsun-Ming Chang, Haiyan Yang, Guiquan Wang, Liangshan Mu","doi":"10.1111/1753-0407.70132","DOIUrl":"https://doi.org/10.1111/1753-0407.70132","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Whether diverse metabolic statuses within a similar body mass index (BMI) category associate with different in vitro fertilization (IVF) outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Design</h3>\u0000 \u0000 <p>A retrospective cohort study.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Setting</h3>\u0000 \u0000 <p>Wenzhou, Zhengjiang Province, China.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Population</h3>\u0000 \u0000 <p>This retrospective cohort study prescreened 16 458 women who underwent their first IVF and fresh embryo transfer cycle between January 2010 and December 2021.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Metabolic status was assessed using the National Cholesterol Education Program–Adult Treatment Panel III criteria. Patients were then categorized into six groups: metabolically healthy normal weight, metabolically unhealthy normal weight, metabolically healthy overweight, metabolically unhealthy overweight, metabolically healthy obese, and metabolically unhealthy obese.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Main Outcome Measures</h3>\u0000 \u0000 <p>The primary outcome was live birth rate.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Regarding live birth, rates in normal weight women were initially lower for metabolically unhealthy normal weight versus metabolically healthy normal weight (44.6% vs. 48.6%), but this was not significant after multivariate adjustment. In obese women, live birth rates were similar between metabolically unhealthy obese and metabolically healthy obese (41.5% vs. 43.9%), with no adjusted difference. For secondary outcomes, metabolically unhealthy normal weight patients had lower biochemical pregnancy rates than metabolically healthy normal weight (OR: 0.86, 95% CI: 0.76–0.98); high blood pressure was a significant risk factor for this outcome in metabolically unhealthy normal weight (OR: 0.84, 95% CI: 0.72–0.98).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our findings indicated that different cardio-metabolic risk factors but a similar BMI category may have limited adverse effects on live birth rate.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70132","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758467","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}
Jimmy Wen, Ubaid Ansari, Mouhamad Shehabat, Zaid Ansari, Burhaan Syed, Adam Razick, Daniel Razick, Muzammil Akhtar, Eldo Frezza
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have demonstrated substantial weight loss effects among patients with diabetes and obesity. However, given the rapid weight loss induced, there is concern about the total change in body composition, including lean body mass (LBM). Current literature on these effects contains significant heterogeneity, with some studies reporting a loss of 40%–60% of LBM and others reporting 15% or less. To combat this, selective androgen receptor modulators (SARMs) have become a popular candidate. Given their androgen receptor selectivity, SARMs have notable anabolic properties and proposed improved safety profiles over traditional anabolic compounds. Several of these agents, such as enobosarm, have been investigated in clinical trials involving older patient populations or patients with cachexia or sarcopenia secondary to chronic diseases. Furthermore, other agents to maintain or enhance LBM, such as antimyostatin agents, are also under investigation. Exploring this potential synergy could lead to better weight loss and body composition management in patients using GLP-1 RAs for diabetes or weight loss therapy. This review aims to evaluate the potential benefits and uses of SARMs in ameliorating the body composition changes induced by GLP-1 RAs. Other investigational agents to retain or increase muscle mass and the future possibilities of these drugs will be discussed.
{"title":"The Potential of SARMs and Antimyostatin Agents in Addressing Lean Body Mass Loss From GLP-1 Agonists: A Literature Review","authors":"Jimmy Wen, Ubaid Ansari, Mouhamad Shehabat, Zaid Ansari, Burhaan Syed, Adam Razick, Daniel Razick, Muzammil Akhtar, Eldo Frezza","doi":"10.1111/1753-0407.70119","DOIUrl":"https://doi.org/10.1111/1753-0407.70119","url":null,"abstract":"<p>Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have demonstrated substantial weight loss effects among patients with diabetes and obesity. However, given the rapid weight loss induced, there is concern about the total change in body composition, including lean body mass (LBM). Current literature on these effects contains significant heterogeneity, with some studies reporting a loss of 40%–60% of LBM and others reporting 15% or less. To combat this, selective androgen receptor modulators (SARMs) have become a popular candidate. Given their androgen receptor selectivity, SARMs have notable anabolic properties and proposed improved safety profiles over traditional anabolic compounds. Several of these agents, such as enobosarm, have been investigated in clinical trials involving older patient populations or patients with cachexia or sarcopenia secondary to chronic diseases. Furthermore, other agents to maintain or enhance LBM, such as antimyostatin agents, are also under investigation. Exploring this potential synergy could lead to better weight loss and body composition management in patients using GLP-1 RAs for diabetes or weight loss therapy. This review aims to evaluate the potential benefits and uses of SARMs in ameliorating the body composition changes induced by GLP-1 RAs. Other investigational agents to retain or increase muscle mass and the future possibilities of these drugs will be discussed.</p>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70119","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740531","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}
To examine the association between non-traditional lipid parameters and adverse pregnancy outcomes (APOs) in women with gestational diabetes mellitus (GDM) and the mediating role of maternal serum metabolites during pregnancy.
Materials and Methods
This prospective observational study enrolled 399 women with GDM. Multivariate logistic regression was used to examine the association between non-traditional lipid parameters and APOs risk. Additionally, we assessed the mediating role of single and composite maternal serum metabolites during pregnancy using causal mediation analysis and high-dimensional mediation analysis, respectively.
Results
APOs were observed in 12.0% (N = 48) of participants. Seven non-traditional lipid parameters, except for the RC/HDL-C ratio, were associated with APOs risk, with the highest estimate for the atherogenic index of plasma (AIP) (OR = 3.873, 95% CI: 1.079–13.934, p = 0.037) after adjusting for confounders. Maternal metabolic markers mediated these associations, with mediation effect proportions of 21.9%–39.4%. Seven key metabolic markers were identified as potential mediators primarily involved in the biosynthesis of the unsaturated fatty acids pathway. Gene set variation analysis revealed significant differences in the positive regulation of this pathway between the APO and normal pregnancy outcome groups (p = 0.015).
Conclusions
Non-traditional lipid parameters were positively associated with APOs risk in women with GDM. Maternal serum metabolites, predominantly involved in the biosynthesis of unsaturated fatty acids, contribute to these associations.
{"title":"Non-Traditional Lipid Parameters and Risk of Adverse Pregnancy Outcomes in Gestational Diabetes Mellitus: Mediation by Maternal Metabolites","authors":"Jing-yi Guo, Dan-dan Yan, Wei Chen, Su-na Wang, Yan-wei Zheng, Wei-tuo Zhang, Cheng Hu, Ming-juan Luo, Xiang-tian Yu","doi":"10.1111/1753-0407.70118","DOIUrl":"https://doi.org/10.1111/1753-0407.70118","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>To examine the association between non-traditional lipid parameters and adverse pregnancy outcomes (APOs) in women with gestational diabetes mellitus (GDM) and the mediating role of maternal serum metabolites during pregnancy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>This prospective observational study enrolled 399 women with GDM. Multivariate logistic regression was used to examine the association between non-traditional lipid parameters and APOs risk. Additionally, we assessed the mediating role of single and composite maternal serum metabolites during pregnancy using causal mediation analysis and high-dimensional mediation analysis, respectively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>APOs were observed in 12.0% (<i>N</i> = 48) of participants. Seven non-traditional lipid parameters, except for the RC/HDL-C ratio, were associated with APOs risk, with the highest estimate for the atherogenic index of plasma (AIP) (OR = 3.873, 95% CI: 1.079–13.934, <i>p</i> = 0.037) after adjusting for confounders. Maternal metabolic markers mediated these associations, with mediation effect proportions of 21.9%–39.4%. Seven key metabolic markers were identified as potential mediators primarily involved in the biosynthesis of the unsaturated fatty acids pathway. Gene set variation analysis revealed significant differences in the positive regulation of this pathway between the APO and normal pregnancy outcome groups (<i>p</i> = 0.015).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Non-traditional lipid parameters were positively associated with APOs risk in women with GDM. Maternal serum metabolites, predominantly involved in the biosynthesis of unsaturated fatty acids, contribute to these associations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144751305","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}
Chong Zhang, Wenjin Peng, Tianqi Wang, Meng Ning, Yi Chen, Yingwu Liu
Background
In acute coronary syndrome (ACS) patients, the relationship between abnormal glucose metabolism markers, such as the triglyceride-glucose (TyG) index and stress hyperglycemia ratio (SHR), and inflammatory markers remains unclear. Furthermore, their interaction and impact on long-term prognosis have yet to be investigated in clinical cohorts.
Methods
In this study, K-means clustering was performed on the TyG index, SHR, and inflammatory markers, including high mobility group box-1 protein, platelet-derived growth factor, phenylacetylglutamine, lysophosphatidic acid, and citrullinated histone H3. A Cox proportional hazards model was used to assess the association between cluster phenotypes and 1-year major adverse cardiovascular events (MACE) risk in ACS patients.
Results
Among 363 ACS patients, 62 developed MACE during the 1-year follow-up. SHR correlated positively with the TyG index and inflammatory markers. K-means clustering identified two phenotypes: normal glucose metabolism/low inflammation and abnormal glucose metabolism/high inflammation. Multivariable Cox analysis showed the latter was strongly linked to MACE (adjusted hazard ratio: 3.84, 95% confidence interval: 1.93–7.64), and early guideline-directed medical therapy reduced MACE risk in this high-risk group.
Conclusions
ACS patients with abnormal glucose metabolism and high inflammation have a higher long-term MACE risk than those with normal glucose metabolism and low inflammation. Early guideline-directed medical therapy, alongside anti-inflammatory therapy and hypoglycemic agents, may improve long-term outcomes in this high-risk group.
{"title":"Association of Abnormal Glucose Metabolism and Inflammation With Prognosis in Patients With Acute Coronary Syndrome","authors":"Chong Zhang, Wenjin Peng, Tianqi Wang, Meng Ning, Yi Chen, Yingwu Liu","doi":"10.1111/1753-0407.70134","DOIUrl":"https://doi.org/10.1111/1753-0407.70134","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>In acute coronary syndrome (ACS) patients, the relationship between abnormal glucose metabolism markers, such as the triglyceride-glucose (TyG) index and stress hyperglycemia ratio (SHR), and inflammatory markers remains unclear. Furthermore, their interaction and impact on long-term prognosis have yet to be investigated in clinical cohorts.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this study, K-means clustering was performed on the TyG index, SHR, and inflammatory markers, including high mobility group box-1 protein, platelet-derived growth factor, phenylacetylglutamine, lysophosphatidic acid, and citrullinated histone H3. A Cox proportional hazards model was used to assess the association between cluster phenotypes and 1-year major adverse cardiovascular events (MACE) risk in ACS patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 363 ACS patients, 62 developed MACE during the 1-year follow-up. SHR correlated positively with the TyG index and inflammatory markers. K-means clustering identified two phenotypes: normal glucose metabolism/low inflammation and abnormal glucose metabolism/high inflammation. Multivariable Cox analysis showed the latter was strongly linked to MACE (adjusted hazard ratio: 3.84, 95% confidence interval: 1.93–7.64), and early guideline-directed medical therapy reduced MACE risk in this high-risk group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>ACS patients with abnormal glucose metabolism and high inflammation have a higher long-term MACE risk than those with normal glucose metabolism and low inflammation. Early guideline-directed medical therapy, alongside anti-inflammatory therapy and hypoglycemic agents, may improve long-term outcomes in this high-risk group.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70134","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740262","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}
It has been shown that offspring of type 2 diabetic parents have a high risk for developing diabetes and atherosclerosis, but the exact mechanism is unclear. In the present study, the possible association between oxidative stress and subclinical atherosclerosis serum markers in this population was investigated.
Method
LDL/HDL ratio, triglyceride-glucose index (TyG), atherogenic index of plasma (AIP), single-point insulin sensitivity estimator (SPISE) index, oxidized LDL (Ox-LDL), intercellular adhesion molecules (ICAM-1 and E-selectin), as well as the marker of oxidative DNA damage were compared among 150 offspring of diabetic parents (90 normoglycemic and normotolerant offspring, 31 offspring with impaired fasting glucose (IFG), and 29 offspring with impaired glucose tolerance (IGT)), and 40 age-and sex-matched healthy control individuals. The control subjects were among individuals with no family history of diabetes.
Results
All three groups with diabetic parents, that is, norm-offspring, IFG, and IGT groups, had higher serum levels of Ox-LDL, ICAM-1, and 8-hydroxy-2′-deoxyguanosine (8-OHdG) than the controls. In the whole population, ICAM-1 correlated with Ox-LDL, fasting plasma glucose (FPG) and 8-OHdG, and Ox-LDL correlated with LDL/HDL, fasting plasma glucose, TyG index, and 8-OHdG after adjustment for age, sex, and BMI.
Conclusion
This study shows that subclinical atherosclerosis and oxidative DNA damage are present in normotolerant normoglycemic offspring of type 2 diabetic parents, and they progress with impaired fasting glucose and/or impaired glucose tolerance. Also, our results indicate that a marker of subclinical atherosclerosis, ICAM-1, was directly correlated with the DNA damage marker, 8-OHdG.
{"title":"The Association Between Subclinical Atherosclerosis Serum Markers and Oxidative DNA Damage in Normoglycemic Normotolerant Offspring of Diabetic Parents","authors":"Masoumeh Rahimi, Farhad Ghadiri Soufi, Shabnaz Koochakkhani, Behnaz Rahnama Inchehsablagh, Abnoos Azarbad, Masoumeh Mahmoudi, Masoumeh Kheirandish, Farideh Jalali Mashayekhi, Ebrahim Eftekhar","doi":"10.1111/1753-0407.70133","DOIUrl":"https://doi.org/10.1111/1753-0407.70133","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>It has been shown that offspring of type 2 diabetic parents have a high risk for developing diabetes and atherosclerosis, but the exact mechanism is unclear. In the present study, the possible association between oxidative stress and subclinical atherosclerosis serum markers in this population was investigated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>LDL/HDL ratio, triglyceride-glucose index (TyG), atherogenic index of plasma (AIP), single-point insulin sensitivity estimator (SPISE) index, oxidized LDL (Ox-LDL), intercellular adhesion molecules (ICAM-1 and E-selectin), as well as the marker of oxidative DNA damage were compared among 150 offspring of diabetic parents (90 normoglycemic and normotolerant offspring, 31 offspring with impaired fasting glucose (IFG), and 29 offspring with impaired glucose tolerance (IGT)), and 40 age-and sex-matched healthy control individuals. The control subjects were among individuals with no family history of diabetes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>All three groups with diabetic parents, that is, norm-offspring, IFG, and IGT groups, had higher serum levels of Ox-LDL, ICAM-1, and 8-hydroxy-2′-deoxyguanosine (8-OHdG) than the controls. In the whole population, ICAM-1 correlated with Ox-LDL, fasting plasma glucose (FPG) and 8-OHdG, and Ox-LDL correlated with LDL/HDL, fasting plasma glucose, TyG index, and 8-OHdG after adjustment for age, sex, and BMI.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study shows that subclinical atherosclerosis and oxidative DNA damage are present in normotolerant normoglycemic offspring of type 2 diabetic parents, and they progress with impaired fasting glucose and/or impaired glucose tolerance. Also, our results indicate that a marker of subclinical atherosclerosis, ICAM-1, was directly correlated with the DNA damage marker, 8-OHdG.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70133","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740263","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}
Pan Gu, Shuai Zheng, Sijie Zhang, Jie Yuan, Hao Hong, Jinglan Dai, Jingyi Zhao, Kuanfeng Xu, Tao Yang, Qi Fu, Sipeng Shen, Hao Dai
Objective
To identify genetic loci that exhibit potential interactions with smoking status on insulin sensitivity and islet β-cell function within normal glucose tolerance (NGT) populations.
Methods
All participants underwent an OGTT to confirm NGT status, followed by assessments of insulin sensitivity and β-cell function. Analyses were performed in NGT participants from Nanjing (N = 4808) and Jurong (N = 508) for discovery and validation, respectively. Smoking status was categorized into nonsmokers and smokers. After excluding ineligible individuals, a two-stage genome-wide interaction association analysis (GWIS) was conducted in NGT individuals, with the discovery phase (N = 1377) identifying gene–environment interactions and the validation phase (N = 485) confirming significant loci. Subsequent analyses included stratified analysis and expression quantitative trait locus (eQTL) colocalization.
Results
GWIS identified ten SNPs in three loci, including rs4713207 (OR14J1, Pmeta = 3.95 × 10−8) for insulin resistance, rs17708475 (NKAIN2, Pmeta = 4.83 × 10−8) for insulin sensitivity, and rs201613 (MYH3, Pmeta = 1.05 × 10−8) for disposition index. Stratified analyses revealed differential effects of smoking across genotypes at these loci. Specifically, smoking was associated with increased insulin resistance in rs4713207 homozygotes (p = 2.15 × 10−5), while an opposite effect was observed in wild-type individuals (p = 0.022). Colocalization analysis indicated that the smoking-related interaction near rs4713207 is driven by a shared causal variant influencing HCG4 (PP.H4 = 0.70) and ZNF311 (PP.H4 = 0.74) expression in the pancreas.
Conclusions
Our findings reveal gene-smoking interactions that affect insulin sensitivity and β-cell function, providing new insights into the heterogeneity of metabolic phenotypes and advancing personalized risk assessment.
{"title":"Gene-Smoking Interaction in Insulin Sensitivity and β-Cell Function Among Normal Glucose Tolerance Individuals","authors":"Pan Gu, Shuai Zheng, Sijie Zhang, Jie Yuan, Hao Hong, Jinglan Dai, Jingyi Zhao, Kuanfeng Xu, Tao Yang, Qi Fu, Sipeng Shen, Hao Dai","doi":"10.1111/1753-0407.70131","DOIUrl":"https://doi.org/10.1111/1753-0407.70131","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To identify genetic loci that exhibit potential interactions with smoking status on insulin sensitivity and islet β-cell function within normal glucose tolerance (NGT) populations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>All participants underwent an OGTT to confirm NGT status, followed by assessments of insulin sensitivity and β-cell function. Analyses were performed in NGT participants from Nanjing (<i>N</i> = 4808) and Jurong (<i>N</i> = 508) for discovery and validation, respectively. Smoking status was categorized into nonsmokers and smokers. After excluding ineligible individuals, a two-stage genome-wide interaction association analysis (GWIS) was conducted in NGT individuals, with the discovery phase (<i>N</i> = 1377) identifying gene–environment interactions and the validation phase (<i>N</i> = 485) confirming significant loci. Subsequent analyses included stratified analysis and expression quantitative trait locus (eQTL) colocalization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>GWIS identified ten SNPs in three loci, including rs4713207 (<i>OR14J1</i>, <i>P</i><sub>meta</sub> = 3.95 × 10<sup>−8</sup>) for insulin resistance, rs17708475 (<i>NKAIN2, P</i><sub>meta</sub> = 4.83 × 10<sup>−8</sup>) for insulin sensitivity, and rs201613 (<i>MYH3, P</i><sub>meta</sub> = 1.05 × 10<sup>−8</sup>) for disposition index. Stratified analyses revealed differential effects of smoking across genotypes at these loci. Specifically, smoking was associated with increased insulin resistance in rs4713207 homozygotes (<i>p</i> = 2.15 × 10<sup>−5</sup>), while an opposite effect was observed in wild-type individuals (<i>p</i> = 0.022). Colocalization analysis indicated that the smoking-related interaction near rs4713207 is driven by a shared causal variant influencing <i>HCG4</i> (PP.H4 = 0.70) and <i>ZNF311</i> (PP.H4 = 0.74) expression in the pancreas.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our findings reveal gene-smoking interactions that affect insulin sensitivity and β-cell function, providing new insights into the heterogeneity of metabolic phenotypes and advancing personalized risk assessment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70131","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144714801","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}
Hailan Zou, Lingxiang Xie, Jingyi Hu, Rong Zhang, Yanfei Wang, Aimin Xu, Zhiguang Zhou, Xiaoyu Xiao, Yang Xiao
Background
Type 1 diabetes is an autoimmune disease with progressive destruction of insulin-producing β cells in islets of Langerhans of the pancreas. However, the early pathogenic factors triggering the recruitment and activation of innate immune cells remain unclear. A study reported that FABP4 accelerates the onset of type 1 diabetes in NOD mice by inducing the polarization of proinflammatory macrophages and their infiltration into pancreatic islets. Nonetheless, the role of FABP4 in mediating crosstalk between innate immunity and adaptive immunity in T1D is unclear.
Methods
Intraperitoneal injections of streptozotocin were used to establish a type 1 diabetes mouse model. Blood glucose was monitored, and intraperitoneal glucose tolerance test (IPGTT) was conducted to compare glucose homeostasis. The peripheral immune cells were detected using flow cytometry. Mixed lymphocyte reactions were applied to examine the function of FABP4 on antigen-presenting in dendritic cells.
Results
We found that genetic ablation of FABP4 in mice alleviated STZ-induced diabetic damage by reducing diabetogenic T lymphocytes and their production of inflammatory cytokines. In vitro studies, FABP4 deficiency dendritic cells expressed lower properties of CD86 and CD80, showing impaired antigen-presenting functions.
Conclusions
Genetic ablation of FABP4 in mice alleviated STZ-induced diabetic damage by impairing the antigen-presenting function of dendritic cells through downregulating the phosphorylation levels of the ERK and JNK pathways.
{"title":"Fatty Acid Binding Protein 4 Regulates the Antigen-Presenting Function of Dendritic Cells Resulting in T Cell Priming in Streptozotocin-Induced Type 1 Diabetes Mice","authors":"Hailan Zou, Lingxiang Xie, Jingyi Hu, Rong Zhang, Yanfei Wang, Aimin Xu, Zhiguang Zhou, Xiaoyu Xiao, Yang Xiao","doi":"10.1111/1753-0407.70123","DOIUrl":"https://doi.org/10.1111/1753-0407.70123","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Type 1 diabetes is an autoimmune disease with progressive destruction of insulin-producing β cells in islets of Langerhans of the pancreas. However, the early pathogenic factors triggering the recruitment and activation of innate immune cells remain unclear. A study reported that FABP4 accelerates the onset of type 1 diabetes in NOD mice by inducing the polarization of proinflammatory macrophages and their infiltration into pancreatic islets. Nonetheless, the role of FABP4 in mediating crosstalk between innate immunity and adaptive immunity in T1D is unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Intraperitoneal injections of streptozotocin were used to establish a type 1 diabetes mouse model. Blood glucose was monitored, and intraperitoneal glucose tolerance test (IPGTT) was conducted to compare glucose homeostasis. The peripheral immune cells were detected using flow cytometry. Mixed lymphocyte reactions were applied to examine the function of FABP4 on antigen-presenting in dendritic cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We found that genetic ablation of <i>FABP4</i> in mice alleviated STZ-induced diabetic damage by reducing diabetogenic T lymphocytes and their production of inflammatory cytokines. In vitro studies, <i>FABP4</i> deficiency dendritic cells expressed lower properties of CD86 and CD80, showing impaired antigen-presenting functions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Genetic ablation of FABP4 in mice alleviated STZ-induced diabetic damage by impairing the antigen-presenting function of dendritic cells through downregulating the phosphorylation levels of the ERK and JNK pathways.</p>\u0000 </section>\u0000 </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"17 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.70123","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144705382","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号