World Journal of Diabetes最新文献

Background: Non-proliferative diabetic retinopathy (NPDR) poses a significant challenge in diabetes management due to its microvascular changes in the retina. Laser photocoagulation, a conventional therapy, aims to mitigate the risk of progressing to proliferative diabetic retinopathy (PDR).

Aim: To compare the efficacy and safety of multi-spot vs single-spot scanning panretinal laser photocoagulation in NPDR patients.

Methods: Forty-nine NPDR patients (86 eyes) treated between September 2020 and July 2022 were included. They were randomly allocated into single-spot (n = 23, 40 eyes) and multi-spot (n = 26, 46 eyes) groups. Treatment outcomes, including best-corrected visual acuity (BCVA), central macular thickness (CMT), and mean threshold sensitivity, were assessed at predetermined intervals over 12 months. Adverse reactions were also recorded.

Results: Energy levels did not significantly differ between groups (P > 0.05), but the multi-spot group exhibited lower energy density (P < 0.05). BCVA and CMT improvements were noted in the multi-spot group at one-month post-treatment (P < 0.05). Adverse reaction incidence was similar between groups (P > 0.05).

Conclusion: While energy intensity and safety were comparable between modalities, multi-spot scanning demonstrated lower energy density and showed superior short-term improvements in BCVA and CMT for NPDR patients, with reduced laser-induced damage.

This letter discusses the publication by Feng et al. Iodine, selenium, and vitamin D are closely associated with thyroid hormone production in humans; however, the efficacy of selenium and vitamin D supplementation for type 2 diabetes mellitus (T2DM) patients with Hashimoto's thyroiditis (HT) remains controversial. In the retrospective study we discuss herein, the authors highlighted significant improvements in thyroid function, thyroid antibodies, blood glucose, and blood lipid in T2DM patients with HT following addition of vitamin D and selenium to their antidiabetic regimens, underscoring the value of these supplements. Our team is currently engaged in research exploring the relationship between micronutrients and HT, and we have obtained invaluable insights from the aforementioned study. Based on this research and current literature, we recommend a regimen of 4000 IU/day of vitamin D and 100-200 μg/day of selenium for over three months to six months for patients with HT, particularly for those with concurrent T2DM.

Background: Mutations in mitochondrial tRNA (mt-tRNA) genes that result in mitochondrial dysfunction play important roles in type 2 diabetes mellitus (T2DM). We pre-viously reported a large Chinese pedigree with maternally inherited T2DM that harbors novel mt-tRNA ^Trp A5514G and tRNA ^Ser(AGY) C12237T variants, however, the effects of these mt-tRNA variants on T2DM progression are largely unknown.

Aim: To assess the potential pathogenicity of T2DM-associated m.A5514G and m.C12237T variants at genetic, molecular, and biochemical levels.

Methods: Cytoplasmic hybrid (cybrid) cells carrying both m.A5514G and m.C12237T variants, and healthy control cells without these mitochondrial DNA (mtDNA) variants were generated using trans-mitochondrial technology. Mitochondrial features, including mt-tRNA steady-state level, levels of adenosine triphosphate (ATP), mitochondrial membrane potential (MMP), reactive oxygen species (ROS), mtDNA copy number, nicotinamide adenine dinucleotide (NAD⁺)/NADH ratio, enzymatic activities of respiratory chain complexes (RCCs), 8-hydroxy-deo-xyguanine (8-OhdG), malondialdehyde (MDA), and superoxide dismutase (SOD) were examined in cell lines with and without these mt-tRNA variants.

Results: Compared with control cells, the m.A5514G variant caused an approximately 35% reduction in the steady-state level of mt-tRNA ^Trp (P < 0.0001); however, the m.C12237T variant did not affect the mt-tRNA ^Ser(AGY) steady-state level (P = 0.5849). Biochemical analysis revealed that cells with both m.A5514G and m.C12237T variants exhibited more severe mitochondrial dysfunctions and elevated oxidative stress than control cells: ATP, MMP, NAD⁺/NADH ratio, enzyme activities of RCCs and SOD levels were markedly decreased in mutant cells (P < 0.05 for all measures). By contrast, the levels of ROS, 8-OhdG and MDA were significantly increased (P < 0.05 for all measures), but mtDNA copy number was not affected by m.A5514G and m.C12237T variants (P = 0.5942).

Conclusion: The m.A5514G variant impaired mt-tRNA ^Trp metabolism, which subsequently caused mitochondrial dysfunction. The m.C12237T variant did not alter the steady-state level of mt-tRNA ^Ser(AGY), indicating that it may be a modifier of the m.A5514G variant. The m.A5514G variant may exacerbate the pathogenesis and progression of T2DM in this Chinese pedigree.

Diabetes mellitus (DM) and obesity have become public issues of global concern. Bariatric surgery for the treatment of obesity combined with type 2 DM has been shown to be a safe and effective approach; however, there are limited studies that have systematically addressed the challenges of surgical treatment of obesity combined with DM. In this review, we summarize and answer the most pressing questions in the field of surgical treatment of obesity-associated DM. I believe that our insights will be of great help to clinicians in their daily practice.

Recently, the roles of pyroptosis, a form of cell death induced by activated NOD-like receptor protein 3 (NLRP3) inflammasome, in the pathogenesis of diabetic cardiomyopathy (DCM) have been extensively investigated. However, most studies have focused mainly on whether diabetes increases the NLRP3 inflammasome and associated pyroptosis in the heart of type 1 or type 2 diabetic rodent models, and whether various medications and natural products prevent the development of DCM, associated with decreased levels of cardiac NLRP3 inflammasome and pyroptosis. The direct link of NLRP3 inflammasome and associated pyroptosis to the pathogenesis of DCM remains unclear based on the limited evidence derived from the available studies, with the approaches of NLRP3 gene silencing or pharmaceutical application of NLRP3 specific inhibitors. We thus emphasize the requirement for more systematic studies that are designed to provide direct evidence to support the link, given that several studies have provided both direct and indirect evidence under specific conditions. This editorial emphasizes that the current investigation should be circumspect in its conclusion, i.e., not overemphasizing its role in the pathogenesis of DCM with the fact of only significantly increased expression or activation of NLRP3 inflammasome and pyroptosis in the heart of diabetic rodent models. Only clear-cut evidence-based causative roles of NLRP3 inflammasome and pyroptosis in the pathogenesis of DCM can help to develop effective and safe medications for the clinical management of DCM, targeting these biomarkers.

Diabetic cardiomyopathy (DbCM) is a common but underrecognized compli-cation of patients with diabetes mellitus (DM). Although the pathobiology of other cardiac complications of diabetes such as ischemic heart disease and cardiac autonomic neuropathy are mostly known with reasonable therapeutic options, the mechanisms and management options for DbCM are still not fully understood. In its early stages, DbCM presents with diastolic dysfunction followed by heart failure (HF) with preserved ejection fraction that can progress to systolic dysfunction and HF with reduced ejection fraction in its advanced stages unless appropriately managed. Apart from prompt control of DM with lifestyle changes and antidiabetic medications, disease-modifying therapy for DbCM includes prompt control of hypertension and dyslipidemia inherent to patients with DM as in other forms of heart diseases and the use of treatments with proven efficacy in HF. A basic study by Zhang et al, in a recent issue of the World Journal of Diabetes elaborates the potential pathophysiological alterations and the therapeutic role of teneligliptin in diabetic mouse models with DbCM. Although this preliminary basic study might help to improve our understanding of DbCM and offer a potential new management option for patients with the disease, the positive results from such animal models might not always translate to clinical practice as the pathobiology of DbCM in humans could be different. However, such experimental studies can encourage more scientific efforts to find a better solution to treat patients with this enigmatic disease.

Background: The incidence of diabetes mellitus type 1 (DM1) has been rising worldwide because of improvements in diagnostic techniques and improved access to care in countries with lower socioeconomic status. A new anti-CD4 antibody, Tep-lizumab, has been shown to delay the progression of DM1 and is the only medication approved for this indication. However, more information is needed about the safety profile of this drug.

Aim: To identify the odds ratios (OR) of systems-based adverse effects for Teplizumab when compared to Placebo.

Methods: An extensive systematic review was conducted from the inception of the medication until December 31, 2023. All clinical trials and studies that evaluated Teplizumab vs placebo were included in the initial review. The study protocol was designed using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines guidelines and was registered in PROSPERO (ID: CRD42024496169). Crude OR were generated using RevMan Software version 5.4.

Results: After screening and review, 5 studies were selected to determine the risk of adverse effects of teplizumab compared to placebo. A total of 561 patients were included in the study population. Total adverse effects and system-based adverse effects were studied and reported. We determined that patients receiving Teplizumab had a higher risk of developing gastrointestinal (GI) (OR = 1.60, 95%CI: 1.01-2.52, P = 0.04), dermatological (OR = 6.33, 95%CI: 4.05-9.88, P < 0.00001) and hematological adverse effects (OR = 19.03, 95%CI: 11.09-32.66, P < 0.00001). These patients were also significantly likely to have active Epstein-Barr Virus infection (OR = 3.16, 95%CI: 1.51-6.64, P < 0.002). While our data showed that patients receiving Teplizumab did have a higher incidence of total adverse effects vs placebo, this finding did not reach statistical significance (OR = 2.25, 95%CI: 0.80-6.29, P = 0.12).

Conclusion: Our systematic review suggests that Teplizumab patients are at risk for significant adverse effects, primarily related to GI, dermatological, and hematological systems. The total adverse effect data is limited as study populations are small. More studies should be conducted on this medication to better inform the target population of potential adverse effects.

In this review article, we explore the interplay between obstructive sleep apnea (OSA) and type 2 diabetes mellitus (T2DM), highlighting a significant yet often overlooked comorbidity. We delve into the pathophysiological links between OSA and diabetes, specifically how OSA exacerbates insulin resistance and disrupts glucose metabolism. The research examines the prevalence of OSA in diabetic patients and its role in worsening diabetes-related complications. Emphasizing the importance of comprehensive management, including weight control and positive airway pressure therapy, the study advocates integrated approaches to improve outcomes for patients with T2DM and OSA. This review underscores the necessity of recognizing and addressing OSA in diabetes care to ensure more effective treatment and better patient outcomes.