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Conclusion Our study demonstrates the alterations of the abundance and diversity of the intestinal microbiota and the perturbation of metabolites in ZDF rats (fa/fa). We found three potential biomarkers of intestinal microbiota that may lead to perturbation in plasma metabolites. This may prompt new pathogenesis of obesity-related T2DM, but we also need to study further about the causal relationship between intestinal microbe and T2DM, so as to find the target of T2DM treatment or preventive measures. © 2020 Wang et al.Purpose To determine what metabolic abnormalities develop frequently among metabolically healthy adults over time according to different baseline body mass index (BMI) categories. Patients and Methods A prospective cohort study was performed on 10,805 adults, who were metabolically healthy at the time of the 2008 survey. Participants were divided into four groups metabolically healthy obese (MHO), metabolically healthy overweight (MHOW), metabolically healthy normal-weight (MHN), and metabolically healthy underweight (MHU). Modified Poisson regression models were used to evaluate the relationship of BMI with the development of metabolic abnormalities. Association rule mining was used to identify the most frequent abnormalities that developed over time. Results Compared with the MHN group, the adjusted relative risks of the MHO group were 1.57 (95% CI 1.09-2.27) and 2.08 (95% CI 1.59-2.73) for developing elevated fasting glucose and elevated blood pressure, respectively, after adjusting for lifestyle behaviours and dietary factors. At the end of follow-up, 33 (19.1%) MHO subjects and 342 (16.6%) MHOW subjects had elevated blood pressure as the predominant metabolic syndrome component, whereas 236 (9.0%) MHU subjects had elevated plasma glucose. The results were similar after stratification by sex. Conclusion MHO and MHOW subjects developed elevated blood pressure most frequently, and MHU subjects developed elevated blood glucose most commonly, regardless of sex. © 2020 Liu et al.Purpose The purpose of this study was to clarify the association between the NLRC4 gene and the susceptibility and clinical characteristics of type 1 diabetes (T1D) in a Chinese Han population. Patients and Methods A case-control study was performed in a Chinese Han population including 510 classical T1D patients and 531 healthy controls. rs212704 and rs385076 of the NLRC4 gene were genotyped by MassARRAY. The frequency distributions of alleles and genotypes of polymorphisms in the NLRC4 gene were compared by logistic regression and the chi-square test. The relationships between the polymorphisms of the NLRC4 gene and various clinical characteristics were analyzed by Kruskal-Wallis one-way ANOVA. The statistical power was calculated by Quanto software. Results 1) rs385076 of the NLRC4 gene was significantly correlated with the onset age of T1D patients and the positive rate of GADA. The relationship between rs212704 and 2-h postprandial C-peptide was statistically significant. 2) There was no significant difference in the frequency distributions of the genotypes and alleles of rs212704 and rs385076 between T1D patients and controls. 3) rs212704 and rs385076 were not correlated with T1D susceptibility under different genetic models. Conclusion rs212704 was associated with 2-h postprandial C-peptide, while rs385076 of the NLRC4 gene was associated with the onset age and positive rate of GADA in patients with T1D. © 2020 Xu et al.Reduced physical activity rate in people's lifestyle is a global concern associated with the prevalence of health disorders such as obesity and metabolic disturbance. Ample evidence has indicated a critical role of the immune system in the aggravation of obesity. The type, duration, and production of adipose tissue-released mediators may change subsequent inactive lifestyle-induced obesity, leading to the chronic systematic inflammation and monocyte/macrophage (MON/MФ) phenotype polarization. Preliminary adipose tissue expansion can be inhibited by changing the lifestyle. In this context, exercise training is widely recommended due to a definite improvement of energy balance and the potential impacts on the inflammatory signaling cascades. How exercise training affects the immune system has not yet been fully elucidated, because its anti-inflammatory, pro-inflammatory, or even immunosuppressive impacts have been indicated in the literature. A thorough understanding of the mechanisms triggered by exercise can suggest a new approach to combat meta-inflammation-induced metabolic diseases. In this review, we summarized the obesity-induced inflammatory pathways, the roles of MON/MФ polarization in adipose tissue and systemic inflammation, and the underlying inflammatory mechanisms triggered by exercise during obesity. © 2020 Soltani et al.Purpose Type 1 diabetes is associated with high risk of cardiovascular disease (CVD). Reduced levels of circulating progenitor cells (CPCs) and endothelial progenitor cells (EPCs) have been indicated as a risk factor for adverse cardiovascular outcomes and death in people at high cardiovascular risk. [https://www.selleckchem.com/products/prt4165.html click here] The aim of the present study was to evaluate the change in CPCs and EPCs levels in a population of young type 1 diabetic patients treated with intensive insulin regimen over a period of 2 years. Patients and Methods A total of 204 type 1 diabetic patients, of whom 84 treated with insulin pump (CSII) and 120 with multiple daily insulin injections (MDI), completed a 2-year follow-up. Clinical measurements, including the indices of glycemic control and glucose variability, were collected at baseline and after 2 years. Both CPC and EPC cell count were assessed by flow cytometry. Results Mean age of participants was 24.5 years and mean diabetes duration was 13.6 years. After 2 years, we found a significant reduction of HbA1c (-0.3% versus baseline, P less then 0.001), associated with decrease in mean amplitude of glucose excursion (MAGE) (-0.5 mmol/L versus baseline, P less then 0.001), continuous overall net glycemic action (CONGA) (-0.2 mmol/L versus baseline, P=0.006), and blood glucose standard deviation (BGSD) (-0.2 mmol/L versus baseline, P less then 0.001). The number of all EPCs phenotypes, but not CPC cell count, significantly raised up in the entire population, with higher increase in CSII group. MAGE resulted as an independent predictor for increased levels of both CD34+ (P = 0.020) and CD34+KDR+ (P = 0.004) cell count in the whole population. Conclusion Over a 2-year follow-up, young type 1 diabetic patients showed an increase in circulating EPCs levels, which was higher in patients with CSII. Glucose variability resulted as an independent predictor of the raised levels of EPCs in this selected population. © 2020 Longo et al.