Aims/Introduction: The present study aimed to determine the associations between expressions of insulin‐like growth factor‐1 (IGF‐1), tumor necrosis factor‐α (TNF‐α) and vascular endothelial growth factor 165 (VEGF₁₆₅) in serum, and occurrence and development of type 2 diabetic nephropathy (DN).Materials and Methods: A total of 108 patients diagnosed as DN were randomly selected, including 50 patients in the microalbuminuria group, 44 patients in the macroalbuminuria group and 14 patients in the renal insufficiency group. Meanwhile, 97 healthy people were collected as a normal control group. Urinary albumin (UALB) and urine creatinine (Cr) of all participants were measured for 24 h, with their ratio (UALB/Cr) being calculated. Enzyme‐linked immunosorbent assay was used to detect the serum concentrations of IGF‐1, TNF‐α and VEGF₁₆₅.Results: The expressions of serum IGF‐1, TNF‐α and VEGF₁₆₅ in the type 2 DN patients were significantly higher than those in the control group (all P < 0.05). The expressions of serum IGF‐1, TNF‐α and VEGF₁₆₅ in the type 2 DN patients were positively correlated with UALB/Cr (all P < 0.05). As type 2 DN worsened, the expressions of serum IGF‐1, TNF‐α and VEGF₁₆₅ increased, and type 2 DN severity had positive correlations with serum IGF‐1, TNF‐α and VEGF₁₆₅ concentrations (all P < 0.05). There was a positive association between IGF‐1 and TNF‐α, IGF‐1 and VEGF₁₆₅, and TNF‐α and VEGF₁₆₅ (all P < 0.05). Logistic regression analysis showed that IGF‐1 and VEGF₁₆₅ were associated with the progression of DN (both P < 0.05).Conclusions: Elevated expression levels of serum IGF‐1, TNF‐α and VEGF₁₆₅ might exacerbate type 2 DN.

Diabetes mellitus (DM) refers to a group of chronic diseases with global prevalence, characterized by persistent hyperglycemia resulting from various etiologies. DM can harm various organ systems and lead to acute or chronic complications, which severely endanger human well-being. Traditional treatment mainly involves controlling blood sugar levels through replacement therapy with drugs and insulin; however, some patients still find a satisfactory curative effect difficult to achieve. Extensive research has demonstrated a close correlation between enteric dysbacteriosis and the pathogenesis of various types of DM, paving the way for novel therapeutic approaches targeting the gut microbiota to manage DM. Fecal microbiota transplantation (FMT), a method for re-establishing the intestinal microbiome balance, offers new possibilities for treating diabetes. This article provides a comprehensive review of the correlation between DM and the gut microbiota, as well as the current advancements in FMT treatment for DM, using FMT as an illustrative example. This study aims to offer novel perspectives and establish a theoretical foundation for the clinical diagnosis and management of DM.

The pathogenesis of diabetic nephropathy (DN), a primary microvascular complication of diabetes and a leading cause of end-stage renal disease, remains incompletely understood. This study delved into the role and underlying mechanisms of miR-216a-5p in the development of DN. Our initial findings revealed a lower serum level of miR-216a-5p in DN patients (P < 0.05). In vitro experiments, in which high glucose concentrations were used to stimulate human mesangial cells (HMCs), demonstrated a significant increase in the protein level of high mobility group box 1 (HMGB1) and a marked decrease in miR-216a-5p expression (all P < 0.05). Subsequent cell experiments showed that miR-216a-5p enhanced HMC viability, stimulated cell proliferation and inhibited cell apoptosis. It also alleviated the fibrosis and inflammatory response of HMC cells under high glucose conditions (all P < 0.05). A dual-luciferase reporter assay confirmed a direct binding between HMGB1 and miR-216a-5p. Moreover, miR-216a-5p suppressed the expression of HMGB1, as well as its receptor for advanced glycation end products (RAGEs). In summary, miR-216a-5p protects against high glucose-induced HMC injury by targeting the HMGB1/RAGE pathway, providing a new perspective for the subsequent treatment of DN.

Background and Aims: The data for the effect of dietary magnesium (Mg) on hemoglobin glycation index (HGI) is limited. Thus, this study aimed to examine the relationship between dietary Mg and HGI in the general population. Methods and Results Our research used data from the National Health and Nutrition Examination Survey from 2001 to 2002. The dietary intake of Mg was assessed by two 24-h dietary recalls. The predicted HbA1c was calculated based on fasting plasma glucose. Logistic regression and restricted cubic spline models were applied to assess the relationship between dietary Mg intake and HGI. We found a significant inverse association between dietary Mg intake and HGI (β = -0.00016, 95%CI: -0.0003, -0.00003, P = 0.019). Dose-response analyses revealed that HGI decreased with increasing intakes of Mg when reached the point above 412 mg/d. There was a linear dose-response relationship between dietary Mg intake and HGI in diabetic subjects, and there was an L-shape dose-response relationship in non-diabetic individuals. Conclusion Increasing the intake of Mg might help lower the risk associated with high HGI. Further prospective studies are requested before dietary recommendations.

Objective The data for the effect of dietary magnesium (Mg) on hemoglobin glycation index (HGI) is limited. Thus, this study aimed to examine the relationship between dietary Mg and HGI in the general population. Methods Our research used the data from the National Health and Nutrition Examination Survey from 2001 to 2002. The dietary intake of Mg was assessed by two 24-h dietary recalls. The predicted HbA1c was calculated based on fasting plasma glucose. Logistic regression and restricted cubic spline models were applied to assess the relationship between dietary Mg intake and HGI. Results We found a significant inverse association between dietary Mg intake and HGI (β = -0.00016, 95%CI: -0.0003, -0.00003, P = 0.019). Dose-response analyses revealed that HGI decreased with increasing intakes of Mg when reached the point above 412 mg/d. There was a linear dose-response relationship between dietary Mg intake and HGI in diabetic subjects, and there was an L-shape dose-response relationship in non-diabetic individuals. Conclusion Increasing the intake of Mg might protect from HGI. Further prospective studies are requested before dietary recommendations.