Diabetes & Metabolism Journal最新文献

Background: Type 2 diabetes mellitus (T2DM) is common among older adults and may increase the risk of sarcopenia and frailty. This study evaluates the impact of sarcopenia and frailty on 5-year mortality in older adults with T2DM.

Methods: We assessed a cohort study of 447 adults with T2DM who were more than 60 years old. To follow the guidelines set by the European Working Group on Sarcopenia in Older People 2 (EWGSOP 2), we used bioelectrical impedance analysis to measure muscle mass and a handgrip dynamometer to measure muscle strength. We assessed frailty using the Fatigue, Resistance, Ambulation, Illnesses, and Loss of weight (FRAIL) Scale. We categorised the patients into four groups: isolated sarcopenic, isolated alone, both conditions (sarcopenia and frailty), or neither.

Results: The mean age of the patients was 69 years, with 71.6% female. Isolated sarcopenic was present in 11.0%, isolated frail in 22.4%, and sarcopenia and frailty in 9.8%. After adjusting for variables such as age, sex, comorbidities, activities of daily living, glycemic control, and nutritional status, sarcopenia and frailty were found to be significantly associated with an increased risk of 5-year mortality. Isolated frail also significantly predicted mortality (hazard ratio, 2.59; 95% confidence interval, 1.34 to 5.03; P=0.005).

Conclusion: Sarcopenia and frailty are significant predictors of increased mortality risk in older adults with T2DM. Sarcopenia and frailty pose the highest risk. Early identification and targeted interventions for these conditions in older T2DM patients are crucial to improving outcomes.

Backgruound: Diabetes often leads to microvascular complications, including nephropathy, neuropathy, and retinopathy. Understanding the impact of early-life factors like birth weight and modifiable behaviors such as cardiovascular health (CVH) is essential for preventing these complications.

Methods: We included 11,515 participants with diabetes but without microvascular complications at baseline from the UK Biobank Study. CVH was evaluated using the Life's Essential 8 score. Independent and joint associations of birth weight and CVH with microvascular complications were analyzed using Cox proportional hazard models. Two-sample Mendelian randomization (MR) analyses estimated unconfounded associations between birth weight and microvascular complications.

Results: Over a median follow-up of 13.1 years, 3,010 microvascular complications occurred. Compared with normal birth weight (2.5-4.0 kg), low birth weight (LBW; <2.5 kg) was associated with 15% higher risk of diabetic nephropathy (hazard ratio [HR], 1.15; 95% confidence interval [CI], 1.01 to 1.31), but not with neuropathy and retinopathy. High birth weight (>4.0 kg) was not associated with the risk of diabetic microvascular complications. MR analysis confirmed the association between LBW and nephropathy. Adherence to high CVH was associated with a reduced risk of microvascular complications compared to low CVH, regardless of birth weight. The HRs were 0.70 (95% CI, 0.59 to 0.84) for the LBW group and 0.74 (95% CI, 0.68 to 0.80) for the group with birth weight ≥2.5 kg (P for interaction=0.69).

Conclusion: LBW was an independent risk factor for nephropathy among diabetic patients. However, the detrimental effects of LBW might be mitigated by improvement in CVH.

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a progressive spectrum ranging from simple hepatic steatosis to steatohepatitis and fibrosis. Although insulin resistance (IR) plays a central role in metabolic diseases, in the liver, insulin- or substrate-driven de novo lipogenesis (DNL) promotes triglyceride accumulation through multiple complex regulatory mechanisms, including specific transcription factors, regardless of whether IR is primary or not. Elevated free fatty acids, resulting from increased adipose lipolysis, further augment hepatic lipid storage and contribute to IR and the progression of MASLD through lipotoxic intermediates such as diacylglycerols and ceramides, as well as other pathways. Numerous studies have identified DNL as a major, yet modifiable, contributor to MASLD. In addition, zonal differences in hepatic insulin signaling, non-classical insulin signaling pathways, and activation of the mechanistic target of rapamycin complex 1 and protein kinase C pathways appear to be involved in the development of selective hepatic IR. Recently, new pharmacologic agents, including resmetirom, have shown promise in improving steatohepatitis and fibrosis in MASLD. Nevertheless, sustained weight loss through lifestyle modification remains the cornerstone of MASLD prevention and therapy. Further mechanistic understanding of how IR and substrate overload promote DNL and hepatic fat accumulation is critical for developing effective treatments for MASLD.

As the prevalence of type 2 diabetes mellitus continues to rise, the development of effective and sustainable prevention strategies has become a critical public health priority. Evidence from large-scale randomized controlled trials has established that lifestyle modification (LSM) programs can substantially reduce the risk of diabetes in high-risk individuals. However, routine implementation is limited by high intensity, costs, and resource requirements. We summarize major prevention trials and their effectiveness, feasibility, and limitations. Building on these insights, we introduce the Korean Diabetes Prevention Study (KDPS) as a contextually tailored model for the Korean healthcare system. The KDPS-LSM program was designed to integrate cultural and clinical relevance with practical applicability, consisting of a 6-month intensive phase of structured nutrition and lifestyle education followed by a maintenance phase to support long-term adherence. To promote sustainable change, the program incorporates the '10 habit' lifestyle messages, grounded in the transtheoretical model of behavior change, which are designed for easy implementation in daily life. This review underscores the importance of developing culturally appropriate LSM programs that balance effectiveness with feasibility, and suggests that the KDPS-LSM model could serve as a useful foundation for establishing practical diabetes prevention strategies within national healthcare systems.

Backgruound: This study aims to identify the status of continuous glucose monitoring (CGM) use among individuals with type 1 diabetes mellitus (T1DM) in South Korea and to investigate whether age-related disparities exist.

Methods: Individuals with T1DM receiving intensive insulin therapy were identified from the Korean National Health Insurance Cohort (2019-2022). Characteristics of CGM users and non-users were compared, and the prescription rates of CGM and sensor- augmented pump (SAP) or automated insulin delivery (AID) systems according to age groups (<19, 19-39, 40-59, and ≥60 years) were analyzed using chi-square tests. Glycosylated hemoglobin (HbA1c) levels and coefficients of variation (CV) among CGM users were also examined.

Results: Among the 56,908 individuals with T1DM, 10,822 (19.0%) used CGM at least once, and 6,073 (10.7%) used CGM continuously. Only 241 (0.4%) individuals utilized either SAP or AID systems. CGM users were younger than non-users. The continuous prescription rate of CGM was highest among individuals aged <19 years (37.0%), followed by those aged 19-39 years (15.8%), 40-59 years (10.7%), and ≥60 years (3.9%) (P<0.001 for between-group differences). Among CGM users, HbA1c levels decreased from 8.7%±2.4% at baseline to 7.2%±1.2% at 24 months, and CV decreased from 36.6%±11.9% at 3 months to 34.1%±12.7% at 24 months.

Conclusion: Despite national reimbursement for CGM devices, the prescription rates of CGM remain low, particularly among older adults. Given the improvements in HbA1c and CV following CGM initiation, more efforts are needed to increase CGM utilization and reduce age-related disparities.

Background: We determined the precise function of E2F transcription factor 5 (E2F5) on the development of diabetic atherosclerosis (DAS) and the underlying mechanisms.

Methods: Apolipoprotein E-knockout mice were intraperitoneally injected streptozotocin for 5 days and fed a high-fat diet for 12 weeks for establishing an in vivo DAS model. To establish a DAS vascular smooth muscle cells (VSMCs) model, VSMCs were stimulated with fresh medium containing glucose and oxidized low-density lipoprotein. After the final treatment, serum lipids were detected, and aorta tissues were collected for hematoxylin and eosin staining, Western blot, Oil red O staining, and quantitative reverse transcription polymerase chain reaction. The effect of E2F5 on the proliferation, migration, cell cycle, phenotype switching, and cell cycle-related markers of VSMCs were evaluated.

Results: In vivo, the expression of E2F5 was elevated in aorta tissues of DAS mice. The downregulation of E2F5 alleviated the symptoms of DAS in mice. Moreover, E2F5 downregulation inhibited the phenotypic transformation of VSMCs in DAS mice. In vitro, the knockdown of E2F5 inhibited the phenotypic transformation of VSMCs. CyclinE overexpression reversed the inhibitory effect of E2F5 silencing on phenotypic transformation of VSMCs. Additionally, we also found that the treatment of BML-284 significantly attenuated the inhibitory effect of E2F5 silencing on phenotypic transformation of VSMCs.

Conclusion: E2F5 is an injurious factor in the pathogenesis of DAS, and the downregulation of E2F5 could repress VSMCs phenotype switching through inactivating Wnt/β-catenin pathway, and ultimately inhibit the progression of DAS.