Diabetes, Obesity & Metabolism最新文献

Aims: A data-driven cluster analysis in a cohort of European individuals with type 2 diabetes (T2D) has previously identified four subgroups based on clinical characteristics. In the current study, we performed a comprehensive statistical assessment to (1) replicate the above-mentioned original clusters; (2) derive de novo T2D subphenotypes in the Kooperative Gesundheitsforschung in der Region Augsburg (KORA) cohort and (3) describe underlying genetic risk and diabetes complications.

Methods: We used data from n = 301 individuals with T2D from KORA FF4 study (Southern Germany). Original cluster replication was assessed forcing k = 4 clusters using three different hyperparameter combinations. De novo clusters were derived by open k-means analysis. Stability of de novo clusters was assessed by assignment congruence over different variable sets and Jaccard indices. Distribution of polygenic risk scores and diabetes complications in the respective clusters were described as an indication of underlying heterogeneity.

Results: Original clusters did not replicate well, indicated by substantially different assignment frequencies and cluster characteristics between the original and current sample. De novo clustering using k = 3 clusters and including high sensitivity C-reactive protein in the variable set showed high stability (all Jaccard indices >0.75). The three de novo clusters (n = 96, n = 172, n = 33, respectively) adequately captured heterogeneity within the sample and showed different distributions of polygenic risk scores and diabetes complications, that is, cluster 1 was characterized by insulin resistance with high neuropathy prevalence, cluster 2 was defined as age-related diabetes and cluster 3 showed highest risk of genetic and obesity-related diabetes.

Conclusion: T2D subphenotyping based on its sample's own clinical characteristics leads to stable categorization and adequately reflects T2D heterogeneity.

Aims: This study aims to investigate the relationship between long-term visit-to-visit within-person HbA1c variability and hospitalisation outcomes in adults with type 2 diabetes (T2D).

Methods: We conducted a cohort study at a tertiary hospital in Singapore involving people aged 21 to 101 years with T2D who had ≥3 HbA1c tests over 2 years. HbA1c variability was assessed using coefficient of variation (CV), variability independent of the mean (VIM) and HbA1c variability score (HVS). A 1-year follow-up was performed after the last HbA1c measurement to identify all-cause and potentially avoidable hospitalisations (PAH), categorised as overall, acute, chronic and diabetes composites.

Results: The study included 14 923 patients (mean age: 62.9 ± 12.9 years; 55% male). The median HbA1c variability was 8.6% CV (IQR: 5.1-14.3). Higher quartiles of HbA1c variability were associated with greater risks of PAH and all-cause hospitalisations, independent of glycaemic control. Compared to Q1, for example, the risk ratios and 95% confidence intervals for diabetes-related PAH based on HbA1c CV were as follows: Q2, 1.32 (0.93-1.88); Q3, 1.65 (1.18-2.31) and Q4, 2.16 (1.54-3.03). For all-cause hospitalisations, they were as follows: Q2, 0.97 (0.90-1.05); Q3, 1.08 (1.00-1.17) and Q4, 1.16 (1.07-1.26). When stratified by glycaemic control, elevated risk of PAH persisted even in those with optimal glycaemic control. Consistent findings were observed using HbA1c VIM and HVS measures.

Conclusions: In individuals receiving care at specialist outpatient clinics of a tertiary hospital, HbA1c variability is associated with a higher risk of PAH. Comprehensive diabetes management strategies addressing both glycaemic control and variability may offer benefits.

Background: The worldwide prevalence of diabetes is increasing, particularly among older adults. Understanding the association between muscle strength and mortality in this population is crucial for developing targeted exercise recommendations.

Objectives: To assess the prospective association of muscle strength with mortality in older adults with diabetes.

Methods: From the Survey of Health, Ageing and Retirement in Europe (SHARE) study, spanning 28 countries, we included 16 149 diabetic adults aged 50 years and older (mean age 68.2 [standard deviation, SD, 9.2] years). Participants fulfilled two criteria: (1) diabetes diagnosis (ever) and (2) current use of diabetes medication. Muscle strength was assessed using handgrip dynamometry (unit: kg). Using time-varying Cox regression with restricted cubic splines, we determined the prospective association of muscle strength with all-cause and cause-specific mortality, controlling for various confounders.

Results: Over a mean follow-up of 5.9 years (SD 3.8), 2754 participants died (17%). Using the median level of muscle strength as reference (30 kg), lower and higher levels were associated in a curvilinear fashion with higher and lower all-cause mortality risk, respectively. The 10th percentile of muscle strength (17 kg) showed a hazard ratio (HR) of 1.65 (95% confidence interval (CI) 1.53-1.79). The 90th percentile (47 kg) of muscle strength showed a HR of 0.55 (95% CI 0.49-0.63). A somewhat similar pattern, with varying strength of associations, was seen for mortality due to cardiovascular disease (CVD), respiratory disease, severe infectious disease, digestive system disease and cancer.

Conclusion: Muscle strength is gradually and inversely associated with all-cause and cause-specific mortality risk in older adults with diabetes. As muscle strength is highly adaptable to resistance training at all ages, the present findings highlight the importance of improving muscle strength in older adults with diabetes.

Background and aim: Vitamin K deficiency is common in persons with kidney disease, which is a known complication of diabetes. We aimed to assess the association of vitamin K status as reflected by plasma dephosphorylated-uncarboxylated matrix Gla protein (dp-ucMGP) with mortality, cardiovascular disease (CVD) and progression to end-stage kidney disease (ESKD) in persons with type 1 diabetes.

Materials and methods: We analysed plasma dp-ucMGP in stored baseline samples from a cohort of 667 persons with type 1 diabetes (baseline visit: 2009-2011). Information on mortality and CVD was obtained through linkage to registers. Cox-proportional hazards models were applied to estimate hazard ratios (HRs) of mortality, CVD and ESKD per one doubling of dp-ucMGP.

Results: A total of 53 deaths were recorded during follow-up. Persons with higher dp-ucMGP (reflecting lower vitamin K status) had higher mortality in the unadjusted model (HR: 2.06 [95% confidence interval-CI: 1.22-3.45]), but not in the fully adjusted model (HR: 0.88 [95% CI: 0.44-1.73]). Particularly, adjustment for glomerular filtration rate and urinary albumin excretion rate attenuated the HR. A similar pattern was observed in unadjusted models for incidence of CVD (HR: 1.58 [95% CI: 1.03-2.42]) and risk of ESKD (HR: 7.62 [95% CI: 4.25-13.68]). In the fully adjusted models, the HRs became statistically insignificant.

Conclusion: In persons with type 1 diabetes, lower vitamin K status was associated with higher mortality, CVD and progression to ESKD, however, not after adjustment for other risk factors. Interventional studies are needed to elucidate the role of vitamin K in persons with type 1 diabetes.

Aim: To investigate the effect of sarcopenic obesity on the progression of glycaemic status in middle-aged and older adults without diabetes.

Materials and methods: This research involved 4637 participants without diabetes from the China Health and Retirement Longitudinal Study 2011-2015. Sarcopenic obesity at baseline was evaluated based on the Asian Working Group for Sarcopenia 2019 criteria. According to the American Diabetes Association criteria, we used fasting plasma glucose and glycated haemoglobin to define glycaemic status. Cox proportional hazard models were applied to obtain adjusted hazard ratios (HRs) and 95% confidence intervals (CIs).

Results: The mean age of included participants was 58.98 ± 8.82 years, and 45.35% were men. During 18,497 person-years of follow-up, 1743 (37.59%) cases with glycaemic status progression were identified. Compared with participants without sarcopenia and obesity, participants with sarcopenic obesity, but not sarcopenia only or obesity only, exhibited a higher risk of progression from normoglycaemia to diabetes (HR = 2.11; 95% CI: 1.10-4.04). Moreover, participants with sarcopenic obesity (HR = 1.65; 95% CI: 1.04-2.63), sarcopenia only (HR = 1.78; 95% CI: 1.11-2.86), or obesity only (HR = 2.00; 95% CI: 1.29-3.12) had increased the risk of progression from prediabetes to diabetes.

Conclusions: The effect of sarcopenic obesity on the progression of glycaemic status based on fasting plasma glucose and glycated haemoglobin may be more pronounced than that of sarcopenia only or obesity only.

Aim: Diabetes is an independent risk factor for muscle mass loss, with possible mechanisms including impaired insulin signalling and chronic inflammation. The use of a glucagon-like peptide 1 (GLP-1) receptor-based agonist could lead to weight reduction, which might result from the loss of both fat and skeletal muscle. However, the body composition-modifying effects of GLP-1 receptor-based agonists have not been systematically characterized.

Methods: PubMed, EMBASE, the Cochrane Center Register of Controlled Trials for Studies and Clinicaltrial.gov were searched from inception to October 2023. Randomized controlled trials of GLP-1 receptor agonist or glucose-dependent insulinotropic polypeptide/GLP-1 receptor dual agonist, which reported the changes of body composition, were included. The results were computed as weighted mean differences (WMDs) and 95% confidence intervals (CIs) in a random-effects model.

Results: In all, 19 randomized controlled trials were included. When compared with controls, substantial reductions in fat body mass were observed in patients using GLP-1 receptor-based agonist treatment (WMD = -2.25 kg, 95% CI -3.40 to -1.10 kg), with decrease in areas of both subcutaneous fat (WMD = -38.35 cm², 95% CI, -54.75 to -21.95 cm²) and visceral fat (WMD = -14.61 cm², 95% CI, -23.77 to -5.44 cm²). Moreover, greater reductions in lean body mass were also observed in GLP-1 receptor-based agonist users compared with non-users (WMD = -1.02 kg, 95% CI, -1.46 to -0.57 kg), while the changes in lean mass percentage were comparable between GLP-1 receptor-based agonist users and non-users.

Conclusion: Compared with the controls, GLP-1 receptor-based agonist users experienced greater reductions in fat body mass, with body shaping effects in terms of both subcutaneous fat mass and visceral fat mass. Although greater reductions in lean body mass were also observed in GLP-1 receptor-based agonist users, the changes in lean mass percentage were comparable between the users and non-users.