Diabetology & Metabolic Syndrome最新文献

Background: Diabetic Foot Ulcers (DFUs) represent a global healthcare challenge, imposing substantial socioeconomic burdens due to their increasing incidence and associated mortality. This study evaluates the efficacy and safety of external phytotherapy (utilizing various plant-derived compounds, including Chinese herbal medicines and plant-derived liposomes, administered topically) for the treatment of DFUs.

Methods: Relevant studies were identified from major electronic databases (PUBMED, EMBASE, WOS, and the Cochrane Library) that were searched up to April 30, 2024. Randomized controlled trials (RCTs) that evaluated the effects of external phytotherapy for DFUs. The treatment group was treated with external phytotherapy plus conventional treatment, while the control group received conventional treatment alone. Two evaluators independently screened and selected literature, extracted data, and assessed the risk of bias. The outcome measures included complete ulcer healing, ulcer improvement, ulcer area reduction, and healing time. Weighted mean difference (WMD), standardized mean difference (SMD), and relative risk (RR) with 95% confidence intervals (CI) were used for data analysis. Heterogeneity was quantified using I² statistics, with appropriate application of fixed-effects or random-effects models. Methodological quality was ensured through Review Manager and Stata software, complemented by GRADE evidence assessment.

Results: Twenty studies with a total of 1,854 participants were identified. Our analysis suggested that compared with conventional treatment, external phytotherapy significantly enhances complete ulcer healing (RR: 1.84; 95% CI: 1.55 to 2.19), promotes ulcer improvement (RR: 1.32; 95% CI: 1.11 to 1.57), reduces ulcer area (WMD: -1.14; 95% CI: -1.45 to -0.83), and accelerates healing time (WMD: -3.93; 95% CI: -7.48 to -0.39). Safety profiles and ulcer depth measurements showed no significant intergroup differences. GRADE assessments indicated high-certainty evidence for most primary outcomes, whereas the evidence for percentage ulcer reduction was of low certainty due to serious inconsistency and imprecision.

Conclusion: External phytotherapy demonstrates potential as an adjunctive treatment for diabetic foot ulcers, improving primary outcomes like complete healing with moderate to high certainty of evidence. Nevertheless, regional bias-with most evidence derived from East Asia-warrants caution in generalizing these results. Further rigorous, multi-regional trials are needed to solidify the evidence base and refine clinical application.

Background: Patients with type 2 diabetes mellitus (T2DM) undergoing percutaneous coronary intervention (PCI) are at high risk of adverse cardiovascular and renal outcomes. While both sodium-glucose cotransporter-2 inhibitors (SGLT-2i) and dipeptidyl peptidase-4 inhibitors (DPP-4i) are widely used in this population, direct evidence comparing their long-term efficacy and safety after PCI remains scarce. This meta-analysis aimed to compare cardiovascular and renal outcomes between SGLT-2i and DPP-4i in patients with T2DM post-PCI.

Methods: PubMed, Web of Science, Scopus, and Cochrane CENTRAL were searched through June 2025. Primary outcomes were all-cause mortality, worsening renal function, and heart failure. We included primary studies and assessed the quality of studies using Newcastle Ottawa Scale. RevMan software was used to calculate hazard ratios (HR) estimates and 95% confidence intervals (CI) using the random-effects model.

Results: We analyzed the outcomes between SGLT-2i (n = 7,025 patients) and DPP-4i (n = 7,459 patients). The mean age was 62.7 years, and 77.4% were males. SGLT-2i significantly reduced all-cause mortality (HR = 0.65; 95% CI: 0.54-0.79; P < 0.001) and the risk of worsening renal function (HR = 0.15; 95% CI: 0.09-0.26; P < 0.001). They also demonstrated a significant reduction in heart failure events (HR = 0.59; 95% CI: 0.48-0.74; P < 0.001). For myocardial infarction, a non-significant trend toward risk reduction with SGLT-2i was observed (HR = 0.85; 95% CI: 0.72-1.02; P = 0.08). For cerebrovascular accidents and the need for repeat revascularization (PCI/CABG), no significant difference was observed.

Conclusion: SGLT-2i demonstrates more clinical benefits, and current evidence supports its initiation over DPP-4i in T2DM patients after PCI.

Background: Alcohol use disorder (AUD) affects nearly half a billion people globally and is associated with significant physical and psychiatric comorbidities. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), approved for diabetes and obesity, have shown promise in modulating reward-related brain pathways, suggesting potential benefits in the management of AUD.

Methods: This systematic review and meta-analysis, registered in PROSPERO and conducted per PRISMA guidelines, assessed the effects of GLP-1RA use on AUD and alcohol-related outcomes in adults with obesity or type 2 diabetes mellitus. Five databases (PubMed, Embase, Web of Science, Scopus, and Cochrane Library) were searched up to September 30, 2025. Random-effects models were applied, and sensitivity analyses examined result stability. No subgroup or meta-regression analyses were performed owing to the small number of eligible studies.

Results: Five observational cohort studies (three on AUD diagnosis, two on alcohol-related hospitalization) were included, with sample sizes ranging from 4,321 to > 53,000 participants. GLP-1RA use was associated with a 28% lower risk of AUD diagnosis (HR = 0.72, 95% CI 0.59-0.89; I² = 65%). For alcohol-related hospitalization, a non-significant reduction was observed (HR = 0.76, 95% CI 0.57-1.01; I² = 77%). Leave-one-out sensitivity analyses confirmed the direction and magnitude of the AUD finding but highlighted the limited evidence base for hospitalization.

Conclusion: GLP-1RA use was associated with a reduced risk of AUD diagnosis, with a possible but non-significant reduction in alcohol-related hospitalization. Effects may be mediated through modulation of mesolimbic reward pathways and the gut-brain axis. Further large-scale trials are warranted to confirm these findings.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly nonalcoholic fatty liver disease (NAFLD), often coexists with type 2 diabetes mellitus (T2DM) due to shared metabolic pathways such as insulin resistance. Empagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor, may provide hepatic and metabolic benefits. This study evaluated its effects on liver fat, enzymes, fibrosis, metabolic parameters, and inflammation in T2DM with MASLD.

Methods: A systematic review and meta-analysis of randomized controlled trials (RCTs) was performed according to PRISMA guidelines. Primary outcomes included liver fat content, enzymes, and fibrosis markers. Secondary outcomes were metabolic and inflammatory parameters.

Results: Eleven RCTs (n = 3077) were included. Empagliflozin significantly reduced liver fat (MD = -3.11%; 95% CI: -4.12 to -2.11; p < 0.00001) and liver stiffness (MD = -0.43 kPa; p = 0.003), but had no significant effect on AST (-0.27 IU/L; p = 0.89) or GGT (-9.25 IU/L; p = 0.14). It significantly lowered HbA1c (-0.54%; p < 0.0001), fasting glucose (-20.89 mg/dL; p < 0.0001), weight (-2.04 kg; p < 0.0001), and waist circumference (-3.47 cm; p < 0.0001), with a nonsignificant reduction in BMI (-0.77 kg/m²; p = 0.09).Uric acid decreased (-0.41 mg/dL; p < 0.00001), but IL-6 and fibrosis scores (FIB-4, NFS) remained unchanged.

Conclusion: Empagliflozin improves liver fat, stiffness, glycemic control, body weight, and uric acid in T2DM with MASLD, but its effects on fibrosis and inflammation remain uncertain. Larger, long-term histologic trials are needed to confirm these outcomes.

Background: Type 2 diabetes mellitus (T2D) is associated with cardiac dysfunction caused by oxidative stress, inflammation, and fibrosis. Exercise has shown cardioprotective effects in T2D. However, the impact on the Advanced Glycation End Products (AGE) and its receptors remains unclear. In this study, we investigated whether aerobic exercise modulates the AGE signaling pathway in the hearts of diabetic mice and whether it is associated with oxidative and inflammatory damage.

Methods: Male C57BL/6 mice were fed a control (CTL) diet or a high-fat, high-carbohydrate (HFHC) diet to induce T2D. A subset of the T2D mice underwent aerobic training for 12 weeks (T2D EX), whereas the other mice remained sedentary (T2D). Cardiac tissues were analyzed for AGE deposition, AGE receptors expression, oxidative stress markers, cytokine profiles, and histological changes, including fibrosis and inflammation.

Results: Aerobic exercise in T2D mice reduced the cardiac deposition of fluorescent AGEs and CML, decreased RAGE protein and gene expression, downregulated CD36 and galectin-3 receptors, while not affecting GLO-1 detoxification system. Exercise in T2D mice suppressed cardiac inflammation and fibrosis. Improvements in inflammatory profiles included reduced expression of IL-6, TNF-α, and NF-kB. However, markers of oxidative stress, such as malondialdehyde, remained largely unaffected by exercise. Pearson's correlation analysis showed strong associations between AGE signaling pathway components and cardiac fibrosis, inflammation, and oxidative stress parameters.

Conclusions: Aerobic exercise mitigates cardiac changes in T2D by downregulating the AGE signaling pathway and reducing fibrosis and inflammation. These findings highlight the therapeutic potential of exercise in interfering with AGE-mediated mechanisms to alleviate T2D-associated cardiovascular complications.

Background: This study aimed to explore the impact of admission hyperglycemia on clinical outcomes in patients with acute large ischemic stroke undergoing endovascular treatment (EVT).

Methods: Patients with admission blood glucose levels were obtained from a prospective cohort study. We defined admission hyperglycemia as blood glucose levels ≥ 7.8 mmol/L. The primary effectiveness outcome was ordinal modified Rankin Scale (mRS) score at 90 days. Secondary effectiveness outcomes included other clinical outcomes (mRS 0-2, mRS 0-3, mRS 0-4) at 90 days. Safety outcomes were mortality at 90 days, and symptomatic intracerebral hemorrhage (sICH) within 48 h.

Results: Among the 478 patients with recorded admission blood glucose levels, 186 (38.9%) presented with hyperglycemia at admission. Multivariable logistic regression analysis showed a significant inverse association between admission hyperglycemia and the distribution of mRS at 90 days (adjusted odds ratio [aOR], 0.46; 95% CI 0.31-0.67; P < 0.001). Additionally, admission hyperglycemia was significantly associated with increased mortality (aOR, 2.29; 95% CI 1.47-3.57; P < 0.001) and the occurrence of sICH (aOR, 2.08; 95% CI 1.15-3.76; P = 0.015). Restricted cubic spline regression analysis indicated that blood glucose levels exhibited a nonlinear association with sICH, whereas admission hyperglycemia showed a linear relationship with mRS 0-3, mRS 0-2, and mortality.

Conclusions: Our results demonstrated that admission hyperglycemia was associated with poor clinical outcomes in patients with acute large ischemic stroke who underwent EVT. This finding suggests that admission hyperglycemia may serve as a valuable prognostic indicator for EVT outcomes and can help inform timely preventive interventions.