World Journal of Diabetes最新文献

Background: Diabetes and hypertension are metabolic disorders that are becoming more prevalent. Breastfeeding is recommended by the World Health Organization for women who have given birth and have been reported to reduce the risk of chronic diseases potentially. However, there is no systematic review to explore the relationship between breastfeeding and diabetes/hypertension by consolidating all available evidence on the topic.

Aim: To investigate the relationship between breastfeeding and maternal diabetes and hypertension.

Methods: This review included comparative studies investigating the association between breastfeeding and the risk of type 2 diabetes or hypertension in parous women. Non-English-language articles, reviews, editorials, letters, and protocols were excluded. The Medline, EMBASE, PubMed, Web of Science, and Cochrane databases were searched until May 6, 2024. Risk of bias in non-randomized studies-of exposure was used to assess bias in all the included studies. A meta-analysis was conducted to determine the risk of two chronic lactation-related diseases.

Results: Eighteen studies were included. Five studies discussed hypertension, 12 discussed diabetes, and one discussed both. According to a meta-analysis, lactation significantly reduced the risk of postpartum diabetes in women with gestational diabetes mellitus [hazard ratio = 0.64 (95%CI: 0.47-0.89)]. In addition, the meta-analysis produced significant results for postpartum diabetes and hypertension in non-gestational diabetes women, both favoring breastfeeding. However, the risk of bias in most included studies was low or unclear.

Conclusion: Breastfeeding has consistently been shown to be associated with a lower incidence of maternal hypertension and diabetes later in life, even among mothers who experienced gestational diabetes during pregnancy.

In their retrospective study of 298 diabetic patients with renal/ureteral calculi, Zhou et al identified critical predictors for urosepsis using multivariate logistic regression. Key findings revealed female gender (OR = 2.237, P = 0.03), advanced age (OR = 1.05/year, P = 0.002), fever (OR = 2.999, P = 0.015), severe hydronephrosis (OR = 6.129, P = 0.011), and elevated urinary markers-particularly urine leukocytes (U-LEU+++: OR = 66.0, P < 0.001) and glucose (U-GLU+++: OR = 7.248, P = 0.005) as independent risk factors. These readily accessible clinical parameters offer significant potential for early risk stratification in high-risk populations. While this STROBE-adherent study provides actionable insights, limitations include its single-center design and unaddressed antibiotic protocols. Future multicenter validation should assess residual stone impacts and optimize intervention thresholds. This work establishes a foundation for targeted surveillance protocols in diabetic urolithiasis management.

Background: Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease. The disease characteristics, morbidity, and renal function progression rate of patients with DKD are all related to sex. This suggests that sex hormones may play an important role in changing renal function in patients with diabetes. There have been only a few studies on the correlation between sex hormones and DKD, which have contradictory conclusions.

Aim: To investigate the relationship between circulating sex hormone levels and DKD in men and postmenopausal women with type 2 diabetes mellitus (T2DM).

Methods: This retrospective cross-sectional study included 356 patients with T2DM. Pearson or Spearman rank correlation analyses assessed the relationships between sex hormone levels and renal function indices. By adjusting for age, body mass index, systolic blood pressure, diastolic blood pressure, duration of diabetes, use of sodium-glucose cotrasporter-2 inhibitor, use of glucagon-like peptide-1 receptor agonist, hypertension, use of angiotensin-converting enzyme inhibitor/ angiotensin receptor blocker/angiotensin receptor-neprilysin inhibitor, diabetic retinopathy, diabetic peripheral vascular disease, triglyceride, uric acid, and hemoglobin A1c, multiple linear regression and logistic regression analyses were conducted to identify factors influencing the urinary albumin/creatinine ratio (UACR) and DKD.

Results: In men, dehydroepiandrosterone sulfate levels were inversely associated with log-transformed UACR after adjustment for covariate factors [regression coefficient (β) = -0.691, 95% confidence interval (CI): -1.241 to -0.141 for quartile 4 vs quartile 1; P = 0.006 for trend]. Elevated levels of estradiol were positively associated with DKD [odds ratio (OR) = 3.097, 95%CI: 1.083-8.856 for quartile 4 vs quartile 1; P = 0.041 for trend], and higher luteinizing hormone (LH) levels were similarly associated with DKD (OR = 4.164, 95%CI: 1.30-13.330 for quartile 4 vs quartile 1; P = 0.048 for trend). In postmenopausal women, LH levels were positively correlated with log-transformed UACR and DKD (β = 1.039, 95%CI: 0.284-1.794 for quartile 4 vs quartile 1; P = 0.006 for trend and OR = 15.117, 95%CI: 2.191-104.326 for quartile 4 vs quartile 1; P = 0.004 for trend). Follicle-stimulating hormone (FSH) levels were also positively associated with DKD (OR = 9.588, 95%CI: 1.680-54.709 for quartile 4 vs quartile 1; P = 0.014 for trend).

Conclusion: In men with T2DM, elevated levels of estradiol and LH levels were positively associated with increased risk of DKD. In postmenopausal women with T2DM, high FSH and LH levels were positively associated with increased risk of DKD.

Background: Recent evidence manifests that individuals with type 2 diabetes (T2D) are increasingly affected by oral disorders. Although medicinal herbs have shown promise in managing T2D, their benefit in managing periodontitis risk and subsequent healthcare utilization remains uncertain.

Aim: To compare risk of periodontitis and associated ambulatory care utilization among individuals with T2D who did or did not receive add-on medicinal herbs.

Methods: We included individuals aged 20-70 years with newly diagnosis of T2D and being free of periodontitis in 2000 and 2010. Periodontitis events were tracked from cohort entry until December 31, 2013. The association between medicinal herb use and periodontitis risk was assessed by multivariate Cox regression, while differences in periodontitis-related ambulatory care were analyzed using Mann-Whitney U test.

Results: After propensity score matching, 9728 individuals were included in both the herbal and non-herbal groups. Those who used herbs for more than two years experienced a potently lower risk of periodontitis by 52%. Compared to herb users, the non-users substantially incurred higher frequency and cost of periodontitis-related ambulatory visits post-diagnosis, and the costs per ambulatory visit increased with time after periodontitis onset.

Conclusion: The rollout of this study not only tackled the former research gap but also provided an insight that the combination of medicinal herbs may take into account while planning holistic and individualized oral health care for T2D persons.

Background: Diabetic nephropathy (DN) is one of the most serious microvascular complications of type 2 diabetes mellitus (T2DM), and its incidence increases with the global rise in diabetes prevalence. It is the leading cause of chronic kidney disease and end-stage kidney disease. Patients with DN often experience complex metabolic disorders and chronic inflammatory states, which not only accelerate the decline of renal function but are also closely related to complications such as cardiovascular events and osteoporosis (OP), seriously compromising quality of life. With the in-depth research on the gut microbiota and the emergence of concepts such as the "gut-kidney axis" and the "enteric-bone axis", the key roles of the gut microbiota and its metabolites in metabolic disorders, inflammatory responses, and target organ damage have been increasingly recognized. However, the specific role of gut microbiota in the pathogenesis of DN remains to be further explored. The results obtained may provide evidence to better understand the pathogenesis of DN and to identify high-risk populations at an early stage. This research direction is of strategic significance.

Aim: To assess the correlation of the gut microbiota metabolite trimethylamine N-oxide (TMAO) with inflammatory marker levels and OP in patients with DN.

Methods: A total of 115 patients diagnosed with type 2 DN and treated at the Department of Endocrinology, Second Affiliated Hospital of Shandong First Medical University from August 2022 to December 2024 were enrolled in the DN group, and 115 patients with T2DM without nephropathy were included in the T2DM group. The two groups were compared in terms of gastrointestinal microbiota abundance and relative abundance at the genus level; levels of TMAO, inflammatory markers [including C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α)], and bone metabolism markers [including procollagen type I N-terminal propeptide (PINP), β-CrossLaps (β-CTX), and alkaline phosphatase (ALP)]; and lumbar spine and hip bone mineral density (BMD). The correlation of TMAO level with inflammatory factor and bone metabolism indicator levels was further analyzed.

Results: The DN group had higher Chao1 and Simpson indices of gastrointestinal microbiota diversity than the T2DM group, whereas the ACE and Shannon indices were lower (P < 0.05). The relative abundance of Firmicutes was higher, and the relative abundances of Bacteroidetes, Proteobacteria, and Actinobacteria were lower in the DN group than in the T2DM group (P < 0.05). CRP, IL-6, IL-8, TNF-α, and TMAO levels were considerably elevated in the DN group compared to the T2DM group (P < 0.05). Moreover, the DN group had higher levels of bone turnover markers-including PINP, β-CTX, and ALP-but lower lumbar spine and hip BMDs than the T2DM group (P < 0.

Type 2 diabetes mellitus (T2DM) and obesity are growing global pandemics that shares the common characteristic of insulin resistance (IR). IR leads to progressive β-cell failure, worsening T2DM and its cardiovascular complications. Thus, early diagnosis of IR is important to prevent and reverse β-cell dedifferentiation. However, there is a lack of accessible, non-invasive and affordable tools to early diagnose and stratify IR. The gold standard method used in the research setting is the hyperinsulinemic-euglycemic clamp, however it is invasive, laborious, expensive and difficult to apply at a large scale. Hou et al presents a potential novel surrogate biomarker for diagnosing IR in T2DM. Magnetic resonance imaging derived biomarkers can potentially become the accessible and non-invasive alternative to the hyperinsulinemic-euglycemic clamp, enabling the timely diagnosis of IR with potential clinical applications in T2DM treatments and preventative care.

Left ventricular assist devices (LVADs) represent a cornerstone therapy for advanced heart failure. However, their efficacy in patients with type 2 diabetes mellitus (T2DM) is challenged by diabetes-exacerbated complications. To determine optimal pharmacological strategies to mitigate major LVAD-related complications in patients with T2DM. This review provides evidence for pharmacological strategies to mitigate major LVAD-related complications in T2DM, in which endothelial dysfunction (via impaired PI3K/Akt-NO signaling), chronic inflammation, and diabetic nephropathy amplify the risk of thrombosis, bleeding, infection, and right ventricular (RV) failure. For thromboembolism prevention, individualized warfarin management (international normalized ratio: 2.0-3.0) with intensified monitoring is essential, while aspirin omission in magnetically levitated devices (2 trials) reduces bleeding. Phosphodiesterase-5 inhibitors show promise for thrombosis reduction, but require bleeding risk assessment. Glycemic control necessitates the proactive de-escalation of insulin/sulfonylureas post-LVAD owing to improved insulin sensitivity and hypoglycemia risks, favoring SGLT-2 inhibitors/GLP-1 receptor agonists for cardiometabolic benefits. Driveline infection management requires renal-adjusted antimicrobial prophylaxis, culture-directed therapy, and novel approaches for drug-resistant cases. The prevention of RV failure depends on preoperative hemodynamic optimization and post-operative inotropic support. A multidisciplinary approach integrating anticoagulation precision, infection control, glycemic tailoring, and hemodynamic stabilization is critical to counter T2DM-pathophysiology interactions.

Familial androgen insensitivity syndrome (AIS), resulting from inherited mutations in the androgen receptor (AR) gene, has traditionally been examined within the framework of disorders of sex development. However, growing evidence indicates that AR dysfunction also disrupts systemic metabolic homeostasis, predisposing affected individuals to insulin resistance and type 2 diabetes mellitus. This article synthesizes recent advances in genetics, transcriptomics, and physiology to elucidate how AR mutations drive tissue-specific metabolic reprogramming in key organs, including pancreatic β-cells, skeletal muscle, liver, and adipose tissue. Particular attention is given to a newly identified familial AR variant (c.2117A>G; p.Asn706Ser), which not only broadens the known mutational spectrum of AIS but also underscores the clinical importance of early metabolic risk screening in this population. We further examine how pubertal stage, hormone replacement therapy, and sex-specific signaling pathways interact to influence long-term metabolic outcomes. Lastly, we propose an integrative management framework that incorporates genetic diagnosis, endocrine surveillance, and personalized pharmacological strategies aimed at reducing the risk of type 2 diabetes mellitus and cardiometabolic complications in individuals with AIS. Distinct from previous AIS-centered reviews, this work integrates metabolic and endocrine perspectives into the traditional developmental paradigm, offering a more comprehensive understanding of disease risk and translational management.

Background: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) play a key role in managing type 2 diabetes mellitus (T2DM). Transitioning between different GLP-1RA has been proposed as a treatment strategy.

Aim: To investigate switching patterns between GLP-1RA and their impact on glycemic control.

Methods: A retrospective study involving patients with T2DM who initiated GLP-1RA therapy between 2009 and 2021 and transitioned to another GLP-1RA. Baseline glycated hemoglobin (HbA_1c) was defined as the most recent measurement within 1 year prior to switching, and follow-up HbA_1c was the first measurement recorded 4-15 months post-switch.

Results: Among 70654 patients initiating GLP-1RA therapy, 18047 (25.5%) switched regimens. In the 13970 patients with available HbA_1c, levels decreased from 8.5% ± 1.6% to 7.6% ± 1.4% (P < 0.001). HbA_1c decreased in 78.3% (10943/13970) of these patients, with the most frequent improvement observed in those switching from daily to weekly GLP-1RA (81%, 5582/6890).

Conclusion: Switching between GLP-1RAs can serve as a practical alternative to treatment intensification for effectively managing T2DM.

Diabetic neuropathy (DN) and impaired wound healing in diabetic foot ulcers (DFUs) are major complications of diabetes mellitus, driven by complex molecular mechanisms, including epigenetic modifications. Recent research highlights the role of epigenetic markers including DNA methylation, histone modifications, and non-coding RNAs in regulating inflammatory responses, neuronal degeneration, and tissue repair. This review explores the epigenetics of DN and DFUs, emphasizing key regulatory pathways that influence disease progression and wound healing outcomes. Genome-wide DNA methylation studies reveal accelerated epigenetic aging and metabolic memory effects in DN, contributing to sensory neuron dysfunction and neuropathic pain. Epigenetic dysregulation of inflammatory mediators such as Toll-like receptors and the Nod-like receptor family, pyrin domain-containing 3 inflammasome further exacerbates neuronal damage and delays wound healing. Additionally, histone deacetylases play a pivotal role in oxidative stress regulation via the Nrf2 pathway, which is critical for both neuronal protection and angiogenesis in DFUs. Non-coding RNAs, particularly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs, are emerging as central regulators of the epigenetic crosstalk between DN and DFUs. Several miRNAs, including miR-146a-5p and miR-518d-3p, are implicated in neuropathy severity, while lncRNAs such as nuclear enriched abundant transcript 1 modulate angiogenesis and wound repair. Cellular reprogramming of DFU fibroblasts has also been shown to induce pro-healing miRNA signatures, offering potential therapeutic avenues. Furthermore, recent whole-genome and transcriptomic analyses of DFU-derived monocytes and Charcot foot lesions reveal unique epigenetic signatures that may serve as biomarkers for early detection and personalized interventions. This epigenetic interplay between DN and DFU pathogenesis not only enhances our knowledge of disease mechanisms but also opens avenues for targeted epigenetic therapies to improve clinical outcomes.