Diabetes & vascular disease research最新文献

Diabetic neuropathy is a troublesome complication of diabetes mellitus. It affects about 50% of patients with diabetes and may mask symptoms of ischemic conditions. Sudden blockade in blood flow to the limb known as acute limb ischemia (ALI) is a life-threatening disease associated with peripheral artery disease (PAD). Diabetes mellitus predisposes both to ALI and PAD, while also delaying recognition due to diabetic peripheral neuropathy.We report a case of a patient with poorly controlled type 2 diabetes and atrial fibrillation who presented a rare occurrence of painless acute upper limb ischemia. Despite two embolectomies with positive revascularization, ischemia progressed, leading to amputation.In the article we discuss management of the patient and the case's similarity to diabetic foot disease. Our case report highlights the importance of vigilance against diabetes-related complications, which may manifest unusual symptoms and thus mask other dangerous ailments.

BackgroundEarly-onset type 2 diabetes (T2DM), diagnosed before age 40, progresses rapidly and has a higher risk of complications compared to late-onset T2DM. Its global prevalence is rising, but the underlying risk factors are insufficiently understood.ObjectiveThis systematic review and meta-analysis aimed to evaluate risk factors associated with early-onset T2DM to support clinical decision-making and inform preventive strategies.Methods37 studies (cohort, case-control, cross-sectional) were identified from PubMed, Web of Science, and Embase up to October 31, 2024. Data were analyzed using STATA 17.0, and pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Subgroup analyses were performed by region, study type, and sample size.ResultsCompared with normoglycemic individuals, early-onset T2DM was strongly associated with family history of diabetes (OR = 4.54, 95%CI: 2.31-8.90), high BMI (OR = 2.87, 95%CI: 2.22-3.80), maternal gestational diabetes (OR = 3.01, 95%CI: 2.44-3.72), and elevated fasting glucose (OR = 8.73, 95%CI: 4.91-16.92). Subgroup and sensitivity analyses confirmed the robustness of these findings despite persistent heterogeneity. In comparisons with late-onset T2DM, family history (OR = 2.90), male sex (OR = 1.57), and BMI (OR = 1.12 per unit) remained significant risk factors.ConclusionEarly-onset T2DM is shaped by familial, metabolic, and lifestyle determinants. Incorporating these factors into early screening and intervention programs, particularly lifestyle modification in young high-risk populations, is essential to reduce disease burden and delay progression.

ObjectiveWe aimed to explored the association between atherogenic index of plasma (AIP), body mass index (BMI) and stroke risk among people with abnormal glucose metabolism.MethodsThis study included participants with abnormal glucose metabolism from the China Health and Retirement Longitudinal Study (CHARLS). AIP was computed using the formula log (Triglyceride/High-density lipoprotein cholesterol). Participants were categorized into high and low levels based on median values for both AIP and BMI. Logistic regression models were employed to investigate the associations between AIP, BMI, and stroke.ResultsIn the longitudinal analysis, 195 out of 3,682 individuals (5.3%) experienced stroke. Joint effects of AIP and BMI on stroke risk indicated that odds ratios for stroke were 1.41 (0.86-2.31) for high AIP & low BMI group, 1.81 (1.14-2.89) for low AIP & high BMI group, and 2.15 (1.42-3.27) for high AIP & high BMI group when compared to low AIP & low BMI group. A significant interaction was observed between AIP and BMI regarding stroke risk. However, this association appeared diminished within cross-sectional evaluations.ConclusionElevated levels of both AIP and BMI are significantly correlated with an increased risk of stroke among individuals exhibiting abnormal glucose metabolism during longitudinal analysis.

Visceral adiposity is a pivotal pathogenic driver of type 2 diabetes mellitus (T2DM) and its vascular complications. We performed two-sample Mendelian randomization (MR) analyses to examine the causal relationships between visceral adipose tissue (VAT) accumulation and diabetes complications. Single nucleotide polymorphisms (SNPs) specific to VAT accumulation were identified through large-scale genome-wide association studies (GWAS) at genome-wide significance (P < 5 × 10^-8), using the inverse variance weighted (IVW) approach for primary analyses. The MR-IVW random-effects model revealed significant associations between genetically predicted VAT accumulation and increased risks for T2DM complications: multi-organ (OR = 2.58, 95% CI, 2.21-3.03), neurological (OR = 3.58, 95% CI, 2.34-5.47), retinopathy (OR = 2.90, 95% CI, 2.21-3.81), nephropathy (OR = 3.14, 95% CI, 2.23-4.45), and peripheral vascular (OR = 3.32, 95% CI, 2.31-4.76). Consistency across complementary MR methods supported the causal inference. This study provides genetic evidence that VAT accumulation is causally associated with increased risk of multiple T2DM complications, including neurological, ocular, kidney, and peripheral vascular outcomes. Future research should prioritize mechanistic studies to elucidate VAT-driven inflammatory and lipotoxic pathways in diabetic complications.

BackgroundThe SUSTAIN-6 trial showed the cardiovascular disease (CVD) benefits of semaglutide among patients with type 2 diabetes mellitus (T2DM). We estimated the US population eligibility and preventable CVD events from semaglutide.MethodsUS adults with T2DM were selected from the National Health and Nutrition Examination Survey 2011-2020 based on SUSTAIN-6 eligibility criteria. We estimated composite and secondary CVD events from SUSTAIN-6 treated and placebo published event rates multiplied by the weighted US eligible population, the difference being the number of preventable events which was then divided by 2.1 years to provide annualized estimates.ResultsAmong 4755 (projected to 33.6 million [M]) adults with T2DM, 1132 (6.9 million) fit SUSTAIN-6 criteria. Compared to SUSTAIN-6, our sample more likely had female and black patients, shorter diabetes duration, and was less likely with prior CVD. We estimated 75,681 primary outcome CVD events, 128,329 expanded composite CVD events, 72,390 combined nonfatal MI, nonfatal stroke, and all-cause deaths, 36,195 non-fatal stroke events, 85,552 revascularizations, and 75,681 cases of nephropathy could be prevented annually if eligible T2DM subjects were on semaglutide.ConclusionSemaglutide may prevent over 75,000 CVD events annually if provided to eligible T2DM US adults. Efforts to improve use of these therapies are needed.

BackgroundTo evaluate the diagnostic value of lncRNA SNHG14 and miR-493-5p in gestational diabetes mellitus (GDM).MethodsThis study consisted of 128 GDM patients and 125 healthy controls. Dual luciferase reporter assay detected binding of lncRNA SNHG14 and miR-493-5p. ROC was applied to evaluate the diagnostic value of lncRNA SNHG14 and miR-493-5p for GDM. Independent factors affecting GDM were evaluated using logistic regression analysis. The role of lncRNA SNHG14, miR-493-5p in pregnancy outcome in GDM patients was assessed by chi-square tests.ResultsLncRNA SNHG14 has a target-binding relationship with miR-493-5p. LncRNA SNHG14 was significantly higher in GDM patients, while miR-493-5p was significantly lower; both were independent risk factors for GDM development. Blood glucose indices (fasting, 1 h and 2 h postprandial) were positively correlated with lncRNA SNHG14 and negatively correlated with miR-493-5p in GDM patients. LncRNA SNHG14 in combination with miR-493-5p increased the diagnostic efficiency for GDM. LncRNA SNHG14 was significantly associated with neonatal weight and neonatal jaundice. MiR-493-5p was significantly associated with neonatal jaundice.ConclusionLncRNA SNHG14 in combination with miR-493-5p may be an early diagnostic marker of GDM. LncRNA SNHG14 and miR-493-5p are associated with adverse pregnancy outcomes (macrosomia, neonatal jaundice) in patients with GDM.

ObjectivePatients with diabetes are 3-5 times higher at risk for cardiovascular diseases and myocardial infarction (MI). There is a need to find miRNAs and other target genes to reduce mortality rates. The current study aims to find potential miRNAs and target genes among MI patients, MI patients with pre-diabetes (metformin non-users), and MI patients with diabetes (metformin users).MethodThe candidate miRNAs were identified by microarray profiling, and their differential expression was evaluated through real-time polymerase chain reaction (RT-PCR) in control and patient groups. The potential targets for miR-1 and miR-133a were retrieved from the TargetScan, miRWalk, and miRDB databases. The sensitivity and specificity of miRNAs were assessed using receiver operating characteristic (ROC) curve analyses.ResultsMicroarray profiling identified 16 miRNAs with significantly altered expression in all MI patient groups compared with healthy controls. According to this data, two miR-1 and miR-133a (with a high ratio) were selected for further verification. All patient groups exhibited a significant increase in the expression levels of miR-1 and miR-133a. Also, miR-1 and miR-133a levels were lower in metformin-user patients than in non-user patients (p < 0.05). Moreover, interleukins, growth factors, and other related genes were identified as potential targets for miR-1 and miR-133a. The ROC area under the curve (AUC) was 0.973 (95% CI: 0.718-0.884) for circulating miR-1, and 0.969 (95% CI: 0.723-0.876) for miR-133a in patients with diabetes (p < 0.001).ConclusionPrediction of miRNA profiles and network of target genes are valuable in the early diagnosis of MI in individuals without and with diabetes. Metformin treatment is associated with lower expression of MI-related miRNAs, suggesting a potential mechanism for cardiac protection by this agent.

Introduction & ObjectiveLatent autoimmune diabetes mellitus (LADA), a heterogeneous disease, is much more common in society than thought. Although it has been claimed that LADA is similar to type 2 diabetes mellitus (T2DM) from a cardiovascular perspective, there is no clear consensus. In this context, the objective of this study is to assess subclinical dysfunction in the left and right ventricles in patients with LADA using novel tissue Doppler imaging (TDI) parameters.Materials &MethodsThe sample of this observational case-control study consisted of 57 consecutive patients aged between 30 and 70 years who applied to the endocrinology and metabolism outpatient clinics, were diagnosed with LADA, and were referred to the cardiology clinic for echocardiographic (ECHO) evaluation. The control group consisted of 60 healthy volunteers. Participants' demographic and clinical characteristics and laboratory findings were recorded. All participants underwent ECHO using conventional ECHO and TDI. Subclinical left ventricular dysfunction was assessed using the myocardial performance index (MPI) and isovolumic myocardial acceleration (IVA).ResultsThere were no significant differences between the patient and control groups in terms of conventional ECHO parameters. The left ventricular (LV) MPI was significantly higher in the patient group than in the control group (0.54 ± 0.11 vs 0.47 ± 0.07, p = 0.008). There was no significant difference between the groups in right ventricular (RV) MPI (0.49 ± 0.10 vs 0.46 ± 0.70, p = 0.217). IVA was decreased in both ventricles (IVA mitral: 3.03 ± 1.44 vs 3.78 ± 1.66, p = 0.008 and IVA tricuspid: 2.67 ± 0.88 vs 3.42 ± 0.97, p = 0.034). Both LV IVA and RV IVA were found to be significantly correlated with glutamic acid decarboxylase antibodies' (GADA) levels in the negative direction (R = -0.290, p = 0.005 and R = -0.340, p = 0.001).ConclusionsIt was observed that LADA negatively affected the systolic and diastolic functions of both ventricles, with its effect being more pronounced in the left ventricle. Glycemic control and autoantibody titers were found to be correlated with TDI parameters, emphasizing their relevance in assessing cardiac dysfunction.

ObjectiveImpairment of pancreatic β cells is a pathophysiological feature of type 2 diabetes mellitus (T2DM). However, whether abnormally dysregulated miR-454-3p in T2DM is related to the dysfunction of pancreatic β cell remains to be further investigated.MethodsFirst, T2DM patients and healthy subjects were recruited to measure miR-454-3p. Subsequently, pancreatic β cells were cultured with high glucose. The role of miR-454-3p in insulin synthesis, secretion, cell proliferation, and apoptosis were investigated by RT-qPCR, Glucose-stimulated insulin secretion determination, cell counting kit-8, and flow cytometry assays. The target mRNA of miR-454-3p was predicted using bioinformatics software. Then, the targeted binding relationships between the above two factors were verified through RNA Immunoprecipitation and Dual-Luciferase Reporter assays.ResultsThe expression of miR-454-3p was increased in T2DM patients and pancreatic β cells cultured with high glucose. Moreover, miR-454-3p was positively correlated with FPG and HbA1c levels in patients. In cell experiments, miR-454-3p inhibitors significantly improved the function of pancreatic β cells, including increased insulin synthesis and secretion, and promoted proliferation. Moreover, silencing Yy1 reversed the protective effect of miR-454-3p inhibitors on pancreatic β cells.ConclusionmiR-454-3p, which is dysregulated in T2DM, promotes the damage of pancreatic β cells by regulating Yy1, thus aggravating T2DM.