World Journal of Diabetes最新文献

Smoking increases complications and mortality in people with diabetes. Quitting delivers major benefits, but physiological (weight gain, insulin sensitivity shifts) and psychological barriers make cessation harder in this group. Our review article examined strategies tailored to people with diabetes. All smokers with diabetes should receive clear, personalized advice to quit, embedded in routine care. Among the available medications, varenicline has the strongest evidence in this population. Nicotine replacement therapy and bupropion may help but have limited diabetes-specific data, so they should be used with caution. Tobacco harm reduction (e-cigarettes, heated tobacco products) may facilitate switching away from combustible cigarettes and reduce exposure, although the long-term safety and efficacy in diabetes remain uncertain. Glucagon-like peptide-1 receptor agonists can aid weight and glycemic control and may indirectly support cessation. Digital tools (apps, wearables, and remote monitoring) offer real-time support and adherence tracking, although diabetes-specific effectiveness is still being established. Smoking cessation in people with diabetes requires urgent attention. Evidence-based interventions should be integrated into routine care, with particular attention given to early monitoring of glucose, body weight, and blood pressure after quitting, plus structured follow-up. More research should develop and test tailored, long-term strategies for this high-risk group, including pragmatic trials integrating harm reduction and digital support.

Background: Epigenetic regulation of leptin (LEP) plays a critical role in metabolic disorders, yet its promoter methylation patterns in lean diabetic populations remain poorly characterized. Emerging evidence suggests DNA methylation may precede clinical hyperglycemia, offering potential for early risk stratification. While obesity-associated LEP methylation is well-studied, lean Asian populations who exhibit high diabetes prevalence despite lower adiposity, represent an underexplored cohort. This study hypothesizes that LEP promoter methylation in peripheral leukocytes decreases progressively from normoglycemia to prediabetes and type 2 diabetes mellitus (T2DM), correlating inversely with serum LEP levels in lean Chinese adults [body mass index (BMI) < 24 kg/m²].

Aim: To investigate LEP promoter methylation status and its association with serum LEP levels across glycemic states in lean Chinese adults.

Methods: We enrolled 392 participants including 120 normoglycemic controls, 94 prediabetes [44 impaired fasting glucose (IFG)/50 impaired glucose tolerance (IGT)], 178 T2DM aged 40-60 years with BMI < 24 kg/m². Genomic DNA from peripheral leukocytes underwent bisulfite conversion followed by methylation-specific PCR to assess CpG methylation in the LEP promoter. Serum LEP was quantified via enzyme-linked immunosorbent assay, with other parameters measured through standard assays. Statistical analyses included analysis of variance, χ² tests, and Pearson correlation (Bonferroni-corrected P value).

Results: Methylation frequencies declined progressively: 59.2% (controls) reduced to 43.6% (prediabetes; IFG: 38.6%, IGT: 48%) reduced to 31.5% (T2DM) (all P < 0.05 vs controls; T2DM vs IGT: P = 0.030). Serum LEP levels increased significantly in T2DM (16.94 ± 4.19 μg/L) vs controls (11.33 ± 3.10 μg/L; P = 0.002), with intermediate values in prediabetes (IFG: 13.79 ± 3.32 μg/L; IGT: 12.62 ± 4.81 μg/L). A near-perfect inverse correlation between methylation and LEP levels was observed (r = -0.95, 95%CI: -0.97 to -0.92, P < 0.001), persisting after adjusting for age and BMI (β = -0.91, P < 0.001).

Conclusion: LEP promoter hypomethylation parallels worsening glycemic status in lean Chinese adults, suggesting its potential as a blood-based epigenetic biomarker for diabetes progression, pending validation in longitudinal cohorts.

Background: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are increasingly being used to treat type 2 diabetes mellitus (T2DM) and obesity. Although GLP-1RAs delay gastric emptying, their impact on gastric mucosal visibility during upper endoscopy remains uncertain, especially in Asian patients.

Aim: To investigate the association between GLP-1RA treatment and gastric mucosal visibility during upper endoscopy in Asian patients with T2DM.

Methods: The study population included Korean patients who underwent esophagogastroduodenoscopy (EGD) with concomitant GLP-1RA or dipeptidyl peptidase 4 inhibitor (DPP4i) for the treatment of T2DM. A 1:2 propensity score matching between GLP-1RA and DPP4i users resulted in 198 matched patients and 295 matched patients in each group, respectively. Gastric mucosal visibility was assessed by reviewing endoscopy images with a validated scale (POLPREP). In addition, the rates of aborted and repeat EGD and pulmonary aspiration were also assessed.

Results: Of the 493 matched patients, mean body mass index was 26.0 kg/m². The rate of inadequate gastric mucosal visibility (gastric POLPREP score 0 or 1) was significantly higher in GLP-1RA group than matched DPP4i group (8.6% vs 1.4%, P = 0.0007). The rates of aborted EGD and repeat EGD were also significantly higher in GLP-1RA than DPP4i group (7.6% vs 0.7% in both aborted and repeat EGD, P = 0.0011). Multivariable logistic regression revealed GLP-1RA use as an independent risk factor for both inadequate gastric mucosal visibility (odds ratio = 6.143, 95% confidence interval: 2.289, 20.318, P = 0.0008) and aborted EGD (odds ratio = 11.099, 95% confidence interval: 3.172, 63.760, P = 0.0010). Despite gastric residue, no pulmonary aspiration was reported in either group.

Conclusion: GLP-1RA use was associated with a higher risk of inadequate gastric mucosal visibility and aborted and repeat procedures during upper gastrointestinal endoscopy in Korean patients with T2DM while pulmonary aspiration was not observed.

Background: Diabetes mellitus (DM) is a significant risk factor for cardiovascular diseases and can worsen the risk of cardiovascular events among patients with hypertrophic cardiomyopathy (HCM). However, strong evidence is needed to show the impact of DM on all-cause mortality (ACM) and atrial fibrillation (AF), which we explored in this systematic review and meta-analysis.

Aim: To determine the impact of DM on ACM and AF in patients with HCM.

Methods: PubMed, Google Scholar, and EMBASE databases were searched for studies showing the effect of DM on ACM and AF in HCM. A binary random effects model with a 95% confidence interval (CI) was used to pool odds ratios (ORs) for ACM and AF outcomes. Study quality was assessed using the Joanna Briggs Institute's critical appraisal tool and leave-one-out sensitivity analysis. P < 0.05 was considered statistically significant.

Results: Fourteen studies (n = 106138) with a mean age of 61.76 ± 19.84 years and 61.55% males were included in our systematic review; ten studies (n = 102882) were eligible for meta-analysis. In the unadjusted analysis, DM was not significantly associated with ACM (OR = 0.96; 95%CI: 0.43-2.15; P = 0.93). However, after adjustment, DM showed a significant association with higher ACM risk (adjusted OR = 1.37; 95%CI: 1.16-1.61; P < 0.01). DM was significantly associated with AF in both unadjusted (OR = 2.02; 95%CI: 1.14-3.58; P = 0.04) and adjusted analyses (adjusted OR = 2.68; 95%CI: 1.68-4.27; P = 0.01). The Joanna Briggs Institute tool revealed a low risk of bias. Leave-one-out sensitivity analysis, performed by sequentially excluding each study, demonstrated no significant change in the overall effect estimates, indicating the robustness and stability of our results.

Conclusion: DM significantly increased the risk of ACM and AF, highlighting the importance of tighter glycemic control and cardiovascular risk factor modification among patients with HCM.

Background: Only a few cases of diabetes mellitus with concurrent mutations in the mitochondrial MT-TL1 and CEL genes have been reported worldwide. Racial differences may influence mutation frequency, the presentation of symptoms, and disease progression. This case report describes the clinical features, potential genetic mechanisms, and diagnostic complexity of young-onset diabetes mellitus with concurrent m.3243A>G mutation in MT-TL1 and c.1336G>A mutation in CEL. The objective is to inform precise typing, genetic counseling, and personalized treatment of monogenic diabetes mellitus, while expanding the evidence base on rare forms of diabetes mellitus.

Case summary: A 30-year-old man, diagnosed with diabetic ketoacidosis six years earlier, presented with poor response to insulin therapy (glycated hemoglobin, 15.35%), marked wasting (body mass index: 15.06 kg/m²), sensorineural deafness, diabetic retinopathy, and peripheral neuropathy. Whole-exome sequencing revealed concurrent mutations: Mitochondrial MT-TL1 m.3243A>G (heteroplasmy 41.76%) and CEL c.1336G>A. Family investigation identified his mother, who also had diabetes, as a carrier of the CEL mutation, and his sister as harboring both mutations without diabetes.

Conclusion: This case highlights the genetic heterogeneity of monogenic diabetes and expands the known mutational spectrum. Comprehensive genetic testing is recommended to enhance diagnostic accuracy in cases of suspected monogenic diabetes.

A recent study in the World Journal of Diabetes by Yang et al explored how Rheb1 signaling influenced pancreatic β cell fate and its potential as a therapeutic target. This invited commentary by a senior diabetes researcher discussed the findings of Yang et al in the context of current knowledge on β cell biology, providing critical insight into the role of Rheb1 in β cell survival and function and the prospects for diabetes treatment. Key outcomes of the study were interpreted alongside established literature on Rheb1- mechanistic target of rapamycin signaling in islet cells. Rheb1 emerges as a pivotal regulator of β cell growth and insulin secretory function, aligning with evidence that β cell-specific Rheb1 deletion impairs β cell mass and glucose-stimulated insulin secretion. The commentary highlighted how modulating this pathway could preserve or restore the β cell population in diabetes while cautioning about potential off-target effects (e.g. in α cells). Targeting Rheb1 signaling represents a promising new frontier in diabetes therapy to enhance β cell resilience; however, a balanced approach addressing both its benefits and risks is essential. This letter discussed the scientific implications and future research directions needed to translate Rheb1 modulation into clinical application for diabetes.

This editorial comments on the study by Tao et al, emphasizing the scalable diagnostic tool for metabolic dysfunction-associated steatotic liver disease (MASLD) in type 2 diabetes mellitus (T2DM). Classical indices such as the fatty liver index (FLI), hepatic steatosis index (HSI), and non-alcoholic fatty liver disease-liver fat score have provided valuable insights. Still, their predictive accuracy often varies across populations and clinical settings. In Western cohorts, FLI and HSI are widely applied, yet they depend heavily on anthropometric or categorical variables, which limits their sensitivity in Asian populations. The Zhejiang University index (ZJU index), developed in China, integrates fasting glucose, triglycerides, hepatic enzyme ratios, and body mass index into a composite score of insulin resistance. Recent studies show that the ZJU index outperforms FLI and HSI in predicting MASLD among Chinese patients, particularly those with T2DM, where it demonstrates a nonlinear association with disease risk and identifies a critical threshold of 38.87. The ZJU index links to conditions like sarcopenia, sleep apnea, and gallstones, showing its versatility in metabolic health. This editorial compares its performance with other indices and emphasizes the ZJU index as a next-generation tool for MASLD risk stratification globally.