Aims/Introduction Glucagon‐like peptide‐1 receptor agonists (GLP‐1Ras) are widely used to treat type 2 diabetes. They not only reduce glucose, but also have a positive effect on weight loss. However, few studies have reported the effect of GLP‐1Ras on fat distribution. Materials and Methods PubMed, Cochrane, Embase and ClinicalTrials.gov were searched for randomized controlled trials on GLP‐1Ras and type 2 diabetes, published from inception to June 2021. Our main outcomes were the reductions of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT). Other anthropometric outcomes were also assessed. We used the Cochrane Collaboration tools to assess the risk of bias in the included studies. The quality of the evidence was assessed using the Grades of Recommendation, Assessment, Development and Evaluation profiler version 3.6. Review Manager 5.4.1 and Stata 16.0 were used for data analysis. Results A total of 10 studies involving 541 patients were included. Compared with the control groups, the GLP‐1Ras groups showed reductions in VAT (standard mean difference −0.54, 95% confidence interval [CI] −0.92, −0.17, I 2 = 79%, P = 0.005) and SAT (standard mean difference −0.44, 95% CI −0.60, −0.27, I 2 = 44%, P < 0.00001). In addition, bodyweight (weighted mean difference −3.59, 95% CI −4.30, −2.88, I 2 = 0%, P < 0.00001), waist circumference (weighted mean difference −3.09, 95% CI −4.66, −1.52, I 2 = 70%, P = 0.0001) and body mass index (weighted mean difference −1.11, 95% CI −1.35, −0.86, I 2 = 47%, P < 0.00001) were significantly decreased. According to the Grades of Recommendation, Assessment, Development and Evaluation approach, the level of evidence was low or moderate. Conclusion This study highlights that GLP‐1Ras, especially liraglutide and exenatide, might play an active role in fat distribution in patients with type 2 diabetes. After treatment with GLP‐1Ras, both VAT and SAT decreased, and the decrease of VAT was numerically greater than that of SAT.

The aim of this study was to study the quantity change of endothelial progenitor cells (EPCs) in obese rats fed a high-fat-diet and to investigate the correlation of EPC numbers with visfatin. The impact of visfatin on the quantity and function of EPCs were further investigated by cell culture methods. Male Wistar rats were fed on either a standard diet (NC group) or a high-fat diet (HF group) for 16 weeks. Serum visfatin, Lee's index and the protein expression of visfatin in viseral adipose tissue (VAT) were determined. Bone marrow EPCs in 2 groups of rats were isolated, cultured and counted. EPCs primarily cultured from control male Wistar rats were treated with different concentrations of visfatin. The quantity, migration and adhesion capacity of EPCs were evaluated after visfatin treatment. Protein expression of nuclear factor-κB (NF-κB) in the nuclei of EPCs was detected. After 16-week feeding, body weight, serum visfatin, Lee's index and visfatin contents in viseral fat were significantly increased in the HF group compared with NC group (P<0.01 or P<0.05). The quantity of EPCs primarily cultured from rats in HF group was lower than that in NC group. The quantity of EPCs was negatively correlated with serum visfatin levels, visceral fat, fasting blood glucose, HOMA-IR, total cholesterol, triglyceride and body weight (P<0.01). In cultured EPCs, visfatin significantly increased the protein expression of NF-κB in EPC nuclei (P<0.01) in a dose-dependent manner. The migration and adhesion capacity were impaired by visfatin treatment (P<0.01). In conclusion, bone marrow-derived EPCs decrease in number and have impaired migration and adhesion function in high-fat-fed obese rats, along with increased serum visfatin and protein contents in VAT. Visfatin may have an impact on the quantity and function of EPCs through the NF-κB pathway.

No abstract

Background Studies have shown that the high incidence of type 2 diabetes in China is associated with low birth weight and excessive nutrition in adulthood, which occurred during the famine years of the 1950s and 1960s, though the specific molecular mechanisms are unclear. In this study, we proposed a severe maternal caloric restriction during late pregnancy, followed by a post weaning high-fat diet in mice. After weaning, normal and high-fat diets were provided to mice to simulate the dietary pattern of modern society. Methods The pregnant mice were divided into two groups: normal birth weight (NBW) group and low birth weight (LBW) group. After 3 weeks for weaning, the male offspring mice in the NBW and LBW groups were then randomly divided into four subgroups: NC, NH, LC and LC groups. The offspring mice in the NC, NH, LC and LC groups were respectively fed with normal diet, normal diet, high-fat diet and high-fat diet for 18 weeks. After 18 weeks of dietary intervention, detailed analyses of mRNA and protein expression patterns, signaling pathway activities, and promoter methylation states were conducted for all relevant genes. Results After dietary intervention for 18 weeks, the expressions of CD36, Fabp4, PPARγ, FAS, and ACC1 in the skeletal muscle tissue of the LH group were significantly increased compared with the LC and NH groups (P < 0.05). The level of p-AMPK/AMPK in the skeletal muscle tissue of the LH group was significantly decreased compared with the LC and NH groups (P < 0.05). CPT1 and PGC-1α protein expressions were up-regulated in the LH group (P < 0.05) compared to the LC group. Additionally, the DNA methylation levels of the PGC-1α and GLUT4 gene promoters in the skeletal muscle of the LH groups were higher than those of the LC and NH groups (P < 0.05). However, PPARγ DNA methylation level in the LH group was lower than those of the LC and NH groups (P < 0.05). Conclusions LBW combined with high-fat diets may increase insulin resistance and diabetes through regulating the CD36-related Fabp4-PPARγ and AMPK/ACC signaling pathways.

IL-17 and other cytokines have a number of immunomodulatory effects on thyroid cells. The present study investigated the changes and correlations amongst IL-17, NF-κB, IL-6, IL-10, interferon-γ (IFN-γ), TNF-α, IL-2 and IL-4 in patients with different autoimmune thyroid diseases in order to further clarify the pathogenesis of autoimmune thyroid disease. A total of 82 patients with autoimmune thyroid diseases (41 with Graves' disease and 41 with Hashimoto's thyroiditis) and 53 healthy controls were enrolled. All relevant thyroid hormones were detected by electrochemiluminescence analyzer. The serum levels of IL-17 and other cytokines were detected using flow cytometry, NF-κB was detected by ELISA, reverse transcription-quantitative PCR was used to detect the protein expression of various mRNAs, and the correlations between IL-17 and these factors were analyzed. Significant differences occurred amongst all groups. NF-κB, TNF-α, IL-6, IL-17 and their mRNA levels were significantly higher in the healthy controls compared with those in the patients; whereas IFN-γ and IL-10 levels were significantly lower in the healthy controls compared with those in the patients . Correlation analysis showed that the expression levels of IL-17 and its mRNA were significantly positively correlated with the expression levels of NF-κB, IL-6, thyroid peroxidase antibody, thyroid gland globulin, thyroglobulin antibody, TNF-α and IFN-γ, and were also significantly negatively correlated with IL-10 . These findings suggested that IL-17 was elevated in patients with autoimmune thyroid disease and that IL-17 could activate the NF-κB signaling pathway, stimulate the production and release of inflammatory factors such as TNF-α, IL-6 and IFN-γ and participate in the pathogenesis of autoimmune thyroid injury.