World Journal of Diabetes最新文献

Background: The global prevalence of diabetes among adults aged 29-79 years was found to be 10.5%. It is a global public health threat with a rising trend in morbidity and mortality. Poor glycemic control (GC) among patients with type 2 diabetes mellitus (T2DM) is a major determinant of diabetes-related complications. There are limited data on GC and associated factors among patients with T2DM in South West Region, Cameroon.

Aim: To assess GC and identify contributing factors among patients with T2DM in a regional hospital in South West Region, Cameroon.

Methods: A cross-sectional study was conducted from February 2022 to July 2022 among 131 participants in Limbe Regional Hospital who were selected by convenience. Glycated hemoglobin (HbA1c) was measured by ion-exchange chromatography. Sociodemographic, clinical, and lifestyle data were collected, entered into Excel, and exported to Statistical Package for Social Sciences version 22 for analysis. A multivariate logistic regression analysis was conducted to assess the association between explanatory variables and GC. The level of significance was set at P < 0.05.

Results: The mean age was 56 ± 5.1 years. Eighty-eight (67.2%) patients were female. The mean HbA1c was 8.8% ± 1.8%. Poor GC (HbA1c ≥ 7%) was registered in 106 (80.9%; 95% confidence interval: 73.1%-87.3%) participants. Lack of self-monitoring of blood glucose at home was associated with poor GC (adjusted odds ratio: 3.858, 95% confidence interval: 1.262-11.800; P = 0.018).

Conclusion: The majority of patients with T2DM had poor GC. Absence of self-monitoring of blood glucose at home was the main contributing factor for poor GC.

Diabetes is a major global metabolic disorder, with the type 2 diabetes mellitus (T2DM) population in China expected to reach 168 million by 2050. Electroacupuncture (EA) and auricular acupuncture represent safe, accessible, and multi-targeted strategies for glycemic control with strong translational potential. Clinical studies indicate that EA, targeting trunk and limb acupoints, can significantly reduce fasting plasma glucose and glycated hemoglobin. Mechanistically, EA modulates the neuro-endocrine-immune axis, regulates gut microbiota, and activates insulin signaling pathways. Auricular acupuncture, through vagal innervation, may also exert rapid effects on glucose homeostasis via autonomic modulation. The review's objective is to synthesize and critically evaluate current clinical trials and animal studies on EA and auricular acupuncture for glycemic control in diabetes, particularly T2DM, and to highlight translational implications, mechanistic insights, and evidence gaps. This review also emphasizes translational considerations by highlighting species differences between rodents and humans - an underappreciated yet critical factor influencing the clinical applicability of preclinical findings. Through the integration of recent research advances, the present review not only consolidates clinical and preclinical evidence but also advances a deeper mechanistic framework and underscores the importance of species-specific factors in bridging experimental research and patient care. Future progress requires rigorously designed, adequately powered, multicenter randomized controlled trials with standardized protocols to validate efficacy and define their role in precision diabetes management.

Diabetic cardiomyopathy (DCM) has long been considered as a left ventricular (LV) disease with diastolic dysfunction preceding systolic dysfunction in diabetes. However, it is increasingly recognized that the right ventricle (RV) is also affected by diabetes and may be independently responsible for adverse outcomes in diabetic patients with or without LV failure. Yu et al conducted a 30-week longitudinal evaluation of biventricular function and pathology in OVE26 diabetic mice and revealed early diastolic dysfunction preceding systolic decline, suggesting that early LV diastolic impairment precedes the later onset of systolic dysfunction. With age, the animals developed fibrosis, hypertrophy, and pulmonary arterial hypertension in the RV. The purpose of this editorial is to contextualize these findings within the existing literature by highlighting the interplay between cardiac chambers and the vasculature. We also seek to reiterate that DCM is a condition extending beyond left ventricular dysfunction. As the authors note, the right side of the heart may remain "the forgotten ventricle" in diabetic patients. We hope that the mechanisms discussed in this paper will help researchers to understand the pathogenesis of cardiovascular disease in this context and encourage clinicians to be more attentive to the associated clinical symptoms.

We read with great interest the article by Li et al, reporting an observational study on the inflammatory response-mediated bone loss after dental implant surgery in patients with type 2 diabetes mellitus (T2DM). This study provides relevant information for reducing the risk of peri-implantitis after dental implant surgery in T2DM, highlighting the need to bridge the gap between risk identification and effective clinical management. However, the complex etiopathogenetic mechanisms elucidating the association between elevated inflammatory response markers and marginal bone loss in T2DM are not sufficiently clarified. Recent studies suggest that perirenal adipose tissue and alcohol consumption affect bone metabolism, which may contribute to the observed marginal bone loss after dental implant surgery in T2DM. Therefore, further studies using state-of-the-art bone-assessing methodologies are needed to enhance our understanding of the potential covariant effects of perirenal adipose tissue and alcohol consumption on inflammatory response-mediated bone loss after dental implant surgery in T2DM.

Background: Diabetic retinopathy (DR) is a leading cause of vision loss in working-age adults, with prevalence varying by population and reaching ~ 34% in northern India. DR arises from chronic hyperglycemia-driven oxidative stress, inflammation, and microvascular dysfunction. Intercellular adhesion molecule-1 (ICAM-1) is central to leukocyte adhesion and retinal vascular injury; circulating ICAM-1 is elevated in patients and experimental models. Genetic variants in ICAM-1, notably c.1405A>G (rs5498) and c.721G>A (rs1799969), have been examined as risk markers for microvascular complications. Yet associations with DR are inconsistent across ethnicities, and robust data from northern India are limited, underscoring the need for population-specific studies.

Aim: To determine the association of ICAM-1 gene polymorphisms with DR in patients with type 2 diabetes mellitus (T2DM) from northern India.

Methods: The present study included 614 participants: 302 patients with T2DM and DR and 312 patients with T2DM but without DR. The ICAM-1 polymorphism c.1405A>G (rs5498) was analyzed using PCR-restriction fragment length polymorphism, and analysis of c.721G>A (rs1799969) was done using the amplification-refractory mutation system. Further, approximately 10% of samples were validated for both polymorphisms for the observed genotypes by Sanger sequencing. A meta-analysis incorporating nine studies (1844 DR cases and 1595 controls) was also performed to assess the association of ICAM-1 rs5498 with DR risk.

Results: The allele frequency and genotype distribution of ICAM-1 c.1405A>G polymorphism in the DR and control groups were not significant (P = 0.070 and P = 0.120, respectively). The GG genotype revealed a 1.6-fold increased risk of developing retinopathy (odds ratio = 1.61, 95% confidence interval: 1.01-2.58, P = 0.044). However, the AG genotype did not show any significant association (P = 0.643) between DR cases and controls. With c.721G>A in ICAM-1 the onset and progression of retinopathy was not found to be significantly correlated. The meta-analysis revealed no significant association between rs5498 and DR risk in the overall population or in Asians, but a significant association was observed in Caucasians under the allelic and recessive models.

Conclusion: The ICAM-1 rs5498 GG genotype increased retinopathy risk 1.61-fold in northern Indians. Meta-analysis of nine studies found no Asian association; a Caucasian signal warrants caution given limited subgroups and heterogeneity.

Type 2 diabetes mellitus (T2DM) is characterized by two core pathological features: Insulin resistance and β-cell dysfunction, with dyslipidemia and immune dysregulation playing critical roles in its pathogenesis. Ectopic lipid deposition and lipotoxicity, resulting from dysregulated lipid metabolism, drive T2DM progression by reshaping immune microenvironments across multiple organs. Over the past two decades, the concept of "immune-metabolic coupling" has gained widespread recognition: Lipotoxicity activates immune cells through pattern recognition receptors, eliciting chronic low-grade inflammation and systematically disrupting insulin signaling pathways. This process involves key metabolic tissues including adipose tissue, liver, skeletal muscle, pancreatic islets, and the intestine. Free fatty acids, inflammatory mediators, extracellular vesicles, and immune cell trafficking collectively form a cross-organ communication network that perpetuates the progression of T2DM. This review systematically summarizes organ-specific immune alterations and their interactive mechanisms, and emphasizes that future research should focus on elucidating the mediators and pathways of inter-organ crosstalk, as well as the origins and migration routes of immune cells. These insights will provide a theoretical foundation for advancing from mere management of T2DM toward the restoration of immunometabolic homeostasis.

Background: Diabetic neuropathy (DN) is a progressive disorder with limited effective treatment options.

Aim: To identify potential therapeutic targets for DN by integrating plasma proteomic and transcriptomic data.

Methods: A comprehensive analytical framework was developed to identify multi-omics biomarkers of DN. Protein-protein interaction network and Gene Ontology analyses were performed to explore the biological functions of biomarkers. Tier 1 target proteins were further analyzed. Candidate drug prediction and molecular docking studies were conducted to identify potential treatments while assessing the side effects of key target proteins. The mediation of immune cells in the association between proteins and DN was examined through two-step network Mendelian randomization (MR) analysis.

Results: Nine DN-associated proteins were identified by analyzing protein quantitative trait loci from extensive genome-wide association study data. BTN3A1 and MICB were confirmed using MR, summary data-based MR, and colocalization analyses. Of the nine, HSPA1B, PSMB9, BTN3A1, SCGN, NOTUM, and MICB showed negative associations with DN, whereas WARS, BRD2, and CSNK2B were positive. Gene Ontology analysis indicated enrichment in inflammatory response and neuronal injury pathways. BTN3A1 and MICB were identified as Tier 1 targets. Drug prediction and molecular docking analyses indicated cyclosporin A as a potential therapeutic candidate. Two-step network MR analysis showed that MICB mediated DN through human leukocyte antigen-DR++ monocytes. These integrated findings point to an immune-mediated mechanism with translational potential and nominate BTN3A1 and MICB for focused functional validation.

Conclusion: Our integrated multi-omics approach identified two promising therapeutic targets for DN, laying the groundwork for new treatment strategies and enhancing our understanding of MICB's role in DN.

Chronic low-grade inflammation is a major contributor to both the onset and advancement of type 2 diabetes mellitus (T2DM), and its associated microvascular complications, including diabetic nephropathy, retinopathy, and peripheral neuropathy. This review aims to overview the roles of high sensitivity C-reactive protein (hs-CRP), C-reactive protein (CRP), CRP-to-lymphocyte count ratio (CLR), and the CRP-to-albumin ratio (CAR) as biomarkers for assessing systemic inflammation and predicting the development and severity of diabetic chronic microvascular complications. Elevated levels of CRP and hs-CRP have been consistently associated with increased risk of these complications, reflecting ongoing inflammatory processes that contribute to endothelial dysfunction and tissue damage. Furthermore, CAR and CLR, which combine CRP with albumin and lymphocyte counts respectively, offer a more nuanced understanding of the inflammatory and immune response in T2DM patients. While individual studies have demonstrated the clinical relevance of these biomarkers in predicting disease onset and progression, further investigation is needed to establish their utility in clinical practice. This review highlights the potential of these biomarkers for enhancing early detection, risk stratification, and personalized management of diabetic patients, ultimately aiming to improve outcomes and reduce the burden of diabetic chronic microvascular complications.

The Zhejiang University (ZJU) index, which combines body mass index, fasting blood glucose, triglyceride level and alanine aminotransferase/aspartate aminotransferase ratio, can be used to predict metabolic dysfunction-associated steatotic liver disease (MASLD) in patients with type 2 diabetes mellitus (T2DM). The ZJU index of 38.87 has been identified as the key threshold for diagnosing MASLD. The new model for predicting MASLD in T2DM based on ZJU index shows high diagnostic value. While the study is methodologically robust and offers a valuable clinical tool, it is limited by its cross-sectional design, inpatient cohort bias, unadjusted pharmacotherapy effects, and reliance on ultrasound for MASLD diagnosis. Future validation in outpatient settings, incorporating medication data and advanced fibrosis assessment, is crucial to translate this cost-effective biomarker into wide practice.

Background: Previous studies have shown that individuals with type 1 diabetes (T1D) frequently present with reduced fecal elastase levels, suggesting exocrine pancreatic insufficiency. However, the underlying determinants and the longitudinal trajectory of these changes remain poorly understood.

Aim: To evaluate longitudinal changes in fecal elastase among individuals with T1D, identify associated factors, and determine clinical implications.

Methods: Pancreatic exocrine function was evaluated in a cohort of patients with T1D by measuring fecal elastase concentrations (FECs). After a mean follow-up of 8.5 ± 0.5 years, participants were recontacted, and a second stool sample was obtained. At both time points, detailed medical histories were collected, including information on diabetes progression, metabolic control, complications, gastrointestinal symptoms, and nutritional status. The study was approved by the institutional ethics committee, and written informed consent was obtained from all participants.

Results: A total of 106 individuals with T1D (mean age = 46.2 years; 50% male) were enrolled. At baseline, the median FEC was 239.5 µg/g, with 44 participants (41.5%) demonstrating abnormally low levels (< 200 µg/g). Reduced fecal elastase was significantly associated with male sex, diabetes-related complications, particularly retinopathy, and higher glycated hemoglobin levels. No significant differences in gastrointestinal symptoms, body mass index, nor most serum nutritional markers were observed between individuals with normal vs reduced fecal elastase levels. Sixty-six participants completed follow-up. Their median fecal elastase was 171.5 µg/g, with 59.1% presenting levels below 200 µg/g. Paired analysis showed a non-significant decline in FEC s over time. No clinical nor metabolic variables predicted longitudinal changes in FEC independently.

Conclusion: Fecal elastase levels are frequently reduced in individuals with T1D and may show a gradual decline over time. The clinical impact of these changes appears to be limited.