Cardiovascular diabetology. Endocrinology reports最新文献

{"title":"Projected reduction in major adverse cardiovascular events among high-risk U.S. adults with type 2 diabetes eligible for oral semaglutide: a SOUL trial-based analysis using NHANES (1988-2018) cycles.","authors":"Mustafa Al-Jarshawi, Andrew Cole, Rodrigo Bagur, Hao-Yu Wang, Cheng Han Ng, Dahai Yu, Nicholas W S Chew, Mamas A Mamas","doi":"10.1186/s40842-026-00299-z","DOIUrl":"10.1186/s40842-026-00299-z","url":null,"abstract":"<p><p>BACKGROUND: Oral semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1 RA), has been shown to reduce major adverse cardiovascular events (MACE) in high-risk individuals with type 2 diabetes in the SOUL trial. Its potential population-level impact in the United States, however, remains unclear. METHODS: We applied SOUL trial eligibility criteria to U.S. adults in the National Health and Nutrition Examination Survey (NHANES, 1988–2018) to estimate the number eligible for oral semaglutide and the projected reduction in cardiovascular events over 4.5 years. MACE—defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke—was the primary outcome. Event rates and hazard ratios were derived from the SOUL trial and applied to weighted NHANES data. RESULTS: An estimated 6.1 million U.S. adults met eligibility criteria for oral semaglutide. Without treatment, 847,598 MACE events were projected, compared to 728,934 with treatment—corresponding to 118,664 events potentially prevented (14% relative reduction; number needed to treat [NNT] = 55). This included 28,430 cardiovascular deaths (NNT = 254), 83,489 nonfatal myocardial infarctions (NNT = 78), and 24,521 nonfatal strokes (NNT = 284). Cardiovascular benefits were consistent across sex, race/ethnicity, and clinical subgroups. At 50% uptake, and assuming a 15.5% discontinuation rate as observed in the SOUL trial, an estimated 59,332 MACE, 14,215 cardiovascular deaths, 41,744 nonfatal myocardial infarctions, and 12,260 nonfatal strokes could be prevented. CONCLUSIONS: Widespread use of oral semaglutide among eligible U.S. adults with type 2 diabetes could substantially reduce cardiovascular events. These findings support its potential as a scalable, population-level cardiometabolic intervention and highlight the need for system-level strategies to enhance access and uptake. </p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13196176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147990873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progressive loss of glycemic control during chronic DPP-4 inhibitor therapy despite preserved β-cell function: a case report suggesting acquired incretin resistance.","authors":"Sai Prasad, Aarushi Ahuja, Shreya Sharma, Jay Nagda, Shaily Agrawal, Vidhi Parmar, Harsh Vardhan","doi":"10.1186/s40842-026-00296-2","DOIUrl":"10.1186/s40842-026-00296-2","url":null,"abstract":"<p><p>BACKGROUND: Dipeptidyl peptidase-4 (DPP-4) inhibitors are widely prescribed second-line agents for type 2 diabetes mellitus (T2DM). Secondary treatment failure with DPP-4 inhibitors is conventionally attributed to progressive β-cell dysfunction. Acquired resistance to DPP-4 inhibitor therapy, characterised by progressive glycemic deterioration despite preserved endogenous insulin secretion, remains an under-recognised and poorly documented clinical phenomenon. We report a case of secondary DPP-4 inhibitor failure with preserved β-cell function, raising the hypothesis of acquired incretin resistance as an alternative mechanism of treatment failure. CASE PRESENTATION: A 52-year-old non-obese man (body mass index 24.9 kg/m²) with a 4-year history of T2DM developed progressive glycemic deterioration after 22 months of stable glycemic control with metformin and sitagliptin combination therapy. His glycated haemoglobin (HbA1c) increased from 6.7% to 8.4% over an 8-month period, with corresponding elevations in fasting plasma glucose (168 mg/dL) and postprandial glucose (248 mg/dL). Comprehensive evaluation revealed preserved β-cell function with normal fasting insulin (14 µIU/mL), C-peptide (2.1 ng/mL), and homeostatic model assessment of β-cell function (HOMA-β) of 68%. Insulin resistance was mild (HOMA-IR 2.3). Autoimmune markers were negative, hepatic and renal function were normal (AST 28 U/L, ALT 32 U/L, eGFR 92 mL/min/1.73 m²), and secondary causes of hyperglycemia were systematically excluded. Sitagliptin was discontinued and replaced with low-dose basal insulin (insulin glargine 10 units at bedtime) while metformin was continued. At 6-month follow-up, HbA1c decreased to 6.9% without hypoglycemia or weight gain. CONCLUSIONS: This case raises the hypothesis that acquired resistance to DPP-4 inhibitor therapy, potentially mediated by desensitisation of glucagon-like peptide-1 (GLP-1) receptor signalling pathways, may represent an under-recognised mechanism of secondary treatment failure. Although a single case cannot establish causality, this observation may prompt clinicians to consider DPP-4 inhibitor resistance when encountering unexplained glycemic deterioration in non-obese patients with preserved β-cell function. </p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13188456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147978584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electrostatic lipidopathy drives human diabetic heart failure.","authors":"Flobater I Gawargi, Paras K Mishra","doi":"10.1186/s40842-026-00286-4","DOIUrl":"10.1186/s40842-026-00286-4","url":null,"abstract":"<p><p>BACKGROUND: Human diabetic heart failure (diHF) is a major contributor to cardiovascular morbidity and mortality and is characterized by myocardial lipid overload and oxidative injury; however, the specific lipid species and molecular mechanisms driving myocardial dysfunction remain unclear. OBJECTIVE: To identify lipid species and integrated molecular networks underlying human diHF using an untargeted multi-omics approach. METHODS: We performed integrated lipidomic, metabolomic, and proteomic profiling of human diabetic failing hearts and matched non-diabetic controls. Lipidomic and metabolomic analyses were conducted using high-resolution UPLC-MS/MS, and quantitative proteomics was performed using tandem mass tag-based LC-MS/MS. Multivariate modeling, differential abundance testing, pathway enrichment, and cross-platform network integration were used to define coordinated lipid-metabolite-protein signatures associated with diHF. RESULTS: Multi-omics integration identified “electrostatic lipidopathy”, a charge-dependent remodeling of membrane and metabolic lipid species, as a defining feature of diHF. Diabetic hearts exhibited enrichment of negatively charged polyunsaturated phospholipids and sphingolipids together with increased diradylglycerols, ceramides, and lactosylceramides, generating a highly anionic lipid environment consistent with increased susceptibility to lipid peroxidation and ferroptosis-related injury. Metabolomic profiling revealed disruption of the myocardial lipid-energy axis characterized by a pattern consistent with increased fatty-acid influx, acylcarnitine accumulation, incomplete β-oxidation, and metabolic inflexibility. Proteomic remodeling demonstrated coordinated suppression of oxidative phosphorylation, mitochondrial dysfunction, inflammatory activation, and extracellular matrix remodeling. Network analysis linked lipid charge remodeling with mitochondrial energetic failure, oxidative stress, and fibrotic remodeling in diHF myocardium. CONCLUSIONS: Electrostatic lipidopathy represents a previously unrecognized mechanism of diabetic cardiac remodeling. By linking membrane lipid charge architecture with mitochondrial dysfunction, redox imbalance, and inflammatory-fibrotic signaling, these findings highlight lipid charge imbalance and ferroptosis-related vulnerability as potential therapeutic targets in diabetic heart failure. </p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13159190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147871343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes-induced right ventricular remodeling precedes left ventricular remodeling and occurs via a distinct fatty acid uptake pathway.","authors":"Sushumna B Satyanarayana, Jaden S Campbell, Marjie P Schmitt, Jose E Campos, Rammohan Shukla, Donald F Smith, Sreejayan Nair, Danielle R Bruns","doi":"10.1186/s40842-026-00287-3","DOIUrl":"10.1186/s40842-026-00287-3","url":null,"abstract":"<p><p>Diabetes is a major public health concern, with both type 1 (T1D) and type 2 diabetes (T2D) resulting in diabetic cardiomyopathy (DCM). The hallmark of DCM is metabolic inflexibility, characterized by excess uptake of fatty acids (FA). Elevated FA uptake results in an imbalance between uptake and utilization of FA, leading to lipotoxicity, lipid accumulation associated with DCM. Although DCM is defined by left ventricular (LV) dysfunction, recent work has demonstrated that the right ventricle (RV) also remodels in diabetes but through poorly understood mechanisms. The temporal development of LV versus RV dysfunction is unclear, alongside the metabolic mechanisms that underlie ventricular-specific remodeling. Therefore, we set out to quantify the temporal dynamics of RV and LV remodeling in DCM as well as to identify the mechanisms by which the RV uptakes FA. We utilized several mouse models of T2D as well as a large-animal pig model of T1D to gain mechanistic insight into RV remodeling. In two models of T2D, we show that RV remodeling begins early in disease pathogenesis, before changes in LV structure or function. We quantified FA uptake across models of T1D and T2D, performed lipidomics and found that the LV and RV accumulate different lipid species and that the mechanism of uptake of FA is distinct between the ventricles. Unlike the diabetic LV in which the primary FA transporter CD36 is robustly upregulated, CD36 does not appear to be involved in diabetic RV myopathy. Together, we show that the RV remodels before and independently of the LV via distinct FA metabolic mechanisms. Ventricle-specific targeting for DCM therapies is warranted.</p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13141328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The long-term cardiovascular safety and efficacy of glucagon-like peptide-1 (GLP-1) receptor agonists in high-risk cardiovascular populations: a systematic review and meta-analysis.","authors":"Kezia Peter, Ocin Roka, Emma Sepp, Maya Warburton, Jufen Zhang, Simon C Cork","doi":"10.1186/s40842-026-00295-3","DOIUrl":"10.1186/s40842-026-00295-3","url":null,"abstract":"<p><strong>Background: </strong>Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are widely used for the management of type 2 diabetes and obesity, yet their long-term cardiovascular effects in high-risk populations continue to be actively evaluated. Given emerging evidence of both metabolic and direct cardiovascular actions, a comprehensive synthesis of cardiovascular outcome trial data is required to clarify the efficacy and safety of this drug class.</p><p><strong>Methods: </strong>We conducted a systematic review and meta-analysis of randomised, placebo-controlled cardiovascular outcome trials evaluating GLP-1RAs in adults at high cardiovascular risk. Searches of PubMed, Embase (via OVID), and the Cochrane Library were performed for studies published between January 2015 and May 2025, in accordance with PRISMA 2020 guidelines. Eligible trials included ≥ 3,000 participants with a minimum follow-up of 12 months. The primary outcome was major adverse cardiovascular events (MACE). Secondary outcomes included cardiovascular mortality, all-cause mortality, non-fatal myocardial infarction, non-fatal stroke, hospitalisation for heart failure, and adverse events. Hazard ratios (HRs) with 95% confidence intervals (CIs) were pooled using random-effects meta-analysis. Risk of bias was assessed using the Cochrane RoB 2 tool, and certainty of evidence was evaluated using GRADE.</p><p><strong>Results: </strong>Eleven cardiovascular outcome trials comprising 91,490 participants were included, with a mean follow-up of 2.7 years. GLP-1RA treatment was associated with a significant reduction in MACE compared with placebo (HR 0.86, 95% CI 0.81-0.92). Meta-analysis also demonstrated significant reductions in cardiovascular mortality, all-cause mortality, non-fatal myocardial infarction, non-fatal stroke, and hospitalisation for heart failure. GLP-1RAs did not materially increase the risk of severe hypoglycaemia or acute pancreatitis, while gastrointestinal adverse effects were consistently more frequent.</p><p><strong>Conclusions: </strong>GLP-1 receptor agonists significantly reduce major cardiovascular events and mortality in high-risk populations, with a favourable long-term safety profile. These findings support the broader integration of GLP-1RAs into cardiovascular risk reduction strategies beyond glycaemic control.</p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147826385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise volume modulates cardiac protection in a type 2 diabetic rat model: differential effects of high- and low-volume moderate-intensity endurance exercise training on diabetic cardiomyopathy.","authors":"Rob Simons, Ileana Bonilauri, Lotte Vastmans, Lisa Steegen, Ellen Heeren, Vincent Vandenboer, Eline Verghote, Sarah D'Haese, Guido Claessen, Ivo Lambrichts, Beatriz Martín-Fernández, Pieter-Jan Volders, Dominique Hansen, Dorien Deluyker, Virginie Bito","doi":"10.1186/s40842-026-00288-2","DOIUrl":"10.1186/s40842-026-00288-2","url":null,"abstract":"<p><p>BACKGROUND: Cardiomyopathy is a major complication of type 2 diabetes, whose prevalence continues to rise globally. Although major cardiology and endocrinology societies endorse exercise training to reduce cardiovascular risk, the optimal exercise training modality, and specifically the role of exercise volume, in preventing diabetic cardiomyopathy remains unclear. METHODS: Male Sprague Dawley rats were fed a high-sugar diet to induce type 2 diabetes. At diet onset, animals were assigned to high-volume (HVE, N = 7) or low-volume (LVE, N = 8) moderate-intensity treadmill training, performed five days per week for 18 weeks. Sedentary rats served as controls (N = 6). Cardiac function was assessed using conventional echocardiography, strain imaging, and invasive hemodynamics. Plasma analyses were used to identify systemic metabolic status, and ex vivo techniques quantified left ventricular cardiac fibrosis, oxidative stress, hypertrophy, inflammation, and metabolism. RESULTS: After 18 weeks of diet, sedentary rats developed characteristic features of early-stage diabetic cardiomyopathy, accompanied by impaired systolic function and increased interstitial myocardial fibrosis. Conversely, high volumes of moderate-intensity exercise training partially prevented pathological cardiac remodelling by improving cardiac metabolic regulation, reducing oxidative stress, and enhancing both cardiac stress-responses and systemic metabolic control. Lower volumes of exercise training primarily influence oxidative stress and inflammatory pathways, resulting in modest cardioprotective effects and preservation of cardiac function. By contrast, high-volume exercise training elicited more pronounced cardioprotective effects, reflected by a significantly higher ejection fraction, cardiac output, stroke volume index, and global longitudinal strain relative to sedentary controls. CONCLUSION: The progression of diabetic cardiomyopathy appears to be modulated by exercise training volume. Although both volumes preserve cardiac performance, high-volume exercise training elicited more pronounced cardioprotective effects than low-volume exercise training in T2DM rats. These findings emphasise the importance of further considering exercise volume as a critical variable in the optimisation of evidence-based exercise prescriptions for individuals with type 2 diabetes. </p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147826368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thyroid hormone resistance beta and autoimmune thyroid disease - a family case study highlighting diagnostic and therapeutic challenges.","authors":"Mirjana Đukić, Zlata Kovačević, Karin Zibar Tomšić, Emir Muzurović","doi":"10.1186/s40842-026-00291-7","DOIUrl":"10.1186/s40842-026-00291-7","url":null,"abstract":"<p><p>BACKGROUND: Resistance to thyroid hormone (RTH) is a rare endocrine disorder, most commonly caused by mutations in the thyroid hormone receptor β (TRβ) gene, resulting in the RTH beta (RTHβ) subtype. In contrast, autoimmune thyroid disease (AITD) is common. The coexistence of RTHβ with AITD has not been fully clarified. Here, we describe a family in which RTHβ coexists with AITD, highlighting the complex interplay between these disorders. CASE PRESENTATION: A 45-year-old woman, previously for years treated for hyperthyroidism, presented after a decade-long gap in follow-up, reporting palpitations and fatigue. Laboratory evaluation revealed elevated free thyroxine (fT4 34 pmol/L) and free triiodothyronine (fT3 11.8 pmol/L) with inappropriately normal thyroid-stimulating hormone (TSH 1.87 µIU/mL). Thyroid antibodies, anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) were positive, while TSH receptor antibodies (TRAb) was negative. Thyroid ultrasound demonstrated a mildly enlarged gland with clinically insignificant nodules, and Tc-99 m scintigraphy showed normally functioning tissue. Pituitary MRI was normal. The thyrotropin-releasing hormone (TRH) stimulation test demonstrated an exaggerated TSH response, consistent with RTHβ. Genetic testing confirmed a heterozygous pathogenic thyroid hormone receptor β THRB variant. Further evaluation of the patient’s family and genetic testing confirmed RTHβ in her daughter and sister, both of whom also had coexisting AITD. CONCLUSIONS: The clinical phenotype of RTHβ is highly variable, ranging from asymptomatic individuals to features of hypo- or hyperthyroidism. Variable tissue responsiveness underlies the overlapping features of thyroid hormone excess and deficiency seen in RTHβ. Coexisting primary hypothyroidism due to AITD can further complicate the clinical course, creating diagnostic and therapeutic challenges. This overlap presents unique challenges in diagnosis and management, often leading to diagnostic uncertainty and therapeutic difficulties. Management should be patient-centred, emphasising individual assessment, multidisciplinary collaboration, and long-term follow-up to optimise outcomes and quality of life. </p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of cumulative exposure and dynamic change patterns of metabolic syndrome score with cardiometabolic multimorbidity progression among middle-aged and older Chinese adults: a longitudinal analysis based on CHARLS.","authors":"Jingjing Zhang, Xiaoyu Ding, Qiuyi Xia, Jialin Cong, Hairong Zhang, Zhicheng Song, Li Wang, Anye Du, Yuan Yuan","doi":"10.1186/s40842-026-00289-1","DOIUrl":"10.1186/s40842-026-00289-1","url":null,"abstract":"<p><p>BACKGROUND: Cardiometabolic multimorbidity (CMM) leads to adverse health outcomes. Based on data from the China Health and Retirement Longitudinal Study (CHARLS), we aimed to explore the cumulative exposure and dynamic change patterns of metabolic syndrome score (MetSS) with CMM progression among middle-aged and older Chinese adults. METHODS: Age and sex specific MetSS was assessed according to equations which were developed for Chinese. K-means clustering analysis was used to classify MetSS changes, and cumulative MetSS (cuMetSS) was calculated as follows: (MetSS2012 + MetSS2015)/2 × time (2015 − 2012). The progression of CMM was defined starting with CMD-free, developing into first CMD (FCMD), further progressing into CMM. Logistic regression analyses and restricted cubic splines (RCS) were performed to evaluate the association of MetSS with CMM progression in 3 models. Subgroup and interaction analyses were subsequently undertaken to investigate the effect of physical activity on the associations of baseline MetSS, cuMetSS and MetSS change patterns with FCMD and CMM risk, respectively. RESULTS: A total of 3,322 participants were eligible for analysis, of whom 679 experienced FCMD and 101 progressed to CMM. The K-means method classified 4 clusters. Logistic analyses revealed that the risk of CMM both increased with baseline MetSS and cuMetSS increment in all 3 models. Baseline MetSS on continuous scale was not significantly associated with FCMD (all P > 0.05). Yet cuMetSS on continuous scale was significantly associated with increased risk of FCMD when adjusted age and gender (model 1: OR, 95% CI, P: 1.02, 1.01 to 1.03, 0.006), additionally adjusted education, marital status, residence, drinking status, smoking status, BMI and comorbidity (model 2: 1.02, 1.00 to 1.03, 0.008). Further additional adjustment for physical activity (model 3) yielded no statistical significance (P > 0.05). Further subgroup analyses suggested that significance was only noted in subgroups with inactive or vigorous physical activity. CONCLUSIONS: Our findings indicate that cumulative exposure and dynamic change patterns of MetSS were associated with FCMD and CMM, yet there is a modifiable effect of physical activity on the associations of cuMetSS and MetSS change patterns with FCMD risk. </p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13112801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of semaglutide injection in Indian patients with type 2 diabetes mellitus inadequately controlled on metformin: a phase 3, randomized, active-controlled trial (SIZE-DM study).","authors":"Nitin Kapoor, Shehla Shaikh, Saptarshi Bhattacharya, Sanjay Kalra, Sambit Das, Sunil Kota, Vipul Khandelwal, Arindam Naskar, Amol Dange, Sanket Sorate, Mayura Choudhari, Narayan Deogaonkar, Jayashree Shembalkar, Deepak Varade, Shejole Vivek Samadhan, Shrikant Somani, Richa Giri, Jasminder Singh, Rajesh Kumar Palaparthi, Narendra Prasad, Paramesh Shamanna, Santosh Saklecha, Kushal Bangar, Aruna Mangipudi, Mayur Mayabhate, Nitin Kapure, Akhilesh Sharma, Radhakrishna Vaddem, Mukesh Jaiswal","doi":"10.1186/s40842-026-00290-8","DOIUrl":"10.1186/s40842-026-00290-8","url":null,"abstract":"<p><strong>Background: </strong>This study evaluated the efficacy and safety of generic semaglutide compared with innovator Semaglutide in Indian adults with type 2 diabetes mellitus (T2DM).</p><p><strong>Methods: </strong>This Phase 3, multicenter, randomized, active-controlled, non-inferiority trial enrolled 320 adults with T2DM inadequately controlled on metformin. Participants were randomized 1:1 to receive either generic semaglutide (Alkem laboratories Ltd.) or innovator Inj. semaglutide (Novo Nordisk) for 24 weeks in step-wise dose escalation from 0.25 mg/week to 2 mg/week. The primary endpoint was change in HbA1c from baseline to Week 24. Secondary endpoints included changes in fasting and post-prandial glucose, body weight, and proportion of patients achieving HbA1c < 7.0%. Safety assessments included adverse events, hypoglycemia, various laboratory parameters.</p><p><strong>Results: </strong>Of 320 participants randomized, 313 completed the study. Baseline demographic and clinical characteristics were comparable between groups. At Week 24, both treatments achieved significant HbA1c reductions (mean - 2.20%), with generic semaglutide demonstrating non-inferiority to the reference. Reductions in body weight, fasting and post-prandial glucose were similar between arms. A total of 86.62% of participants achieved HbA1c < 7.0%. Safety profiles were comparable, with predominantly mild-to-moderate adverse events and no treatment-related serious adverse events.</p><p><strong>Conclusion: </strong>Generic semaglutide demonstrated non-inferior efficacy and comparable safety to innovator Semaglutide in Indian adults with T2DM inadequately controlled on metformin, offering an effective and accessible therapeutic option in resource-limited settings.</p>","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Epidemiology of cardiovascular disease and diabetes in 2026: expanding prevalence, escalating costs, and the limits of contemporary prevention.","authors":"Gaetano Santulli","doi":"10.1186/s40842-026-00297-1","DOIUrl":"10.1186/s40842-026-00297-1","url":null,"abstract":"","PeriodicalId":521069,"journal":{"name":"Cardiovascular diabetology. Endocrinology reports","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147795944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}