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Objective This study is aimed at investigating whether exenatide (Exe) delays the progression of nonalcoholic fatty liver disease (NAFLD) in C57BL/6 mice by targeting the NLRP3 inflammasome through the autophagy/mitophagy pathway. Methods Thirty male C57BL/6 mice were randomly divided into three groups: control group (n = 10), model group (n = 10), and Exe (exenatide) group (n = 10). Mouse models of NAFLD and diabetes were established using a high-fat diet and streptozocin. Results The levels of fasting blood glucose (FBG), total cholesterol (TC), and triglyceride (TG) in the serum were significantly reduced after Exe treatment. The body weight, liver weight/body weight, and number of lipid droplets in the liver significantly decreased in Exe-treated mice. Treatment with Exe markedly reduced the levels of liver lipids, malondialdehyde (MDA), and alanine aminotransferase (ALT) in serum and livers. The number of autophagosomes increased significantly in the Exe group. The expression of LC3A/B-II/I, Beclin-1, Parkin, and BNIP3L increased significantly, whereas NLRP3 and IL-1β proteins were suppressed after Exe treatment. Conclusion We successfully established a mouse model of NAFLD and diabetes. Exe may reduce oxidative stress injury and inhibit the NLRP3 inflammasome by enhancing the autophagy/mitophagy pathway in liver, which has a protective effect on the liver in NAFLD and diabetes in C57BL/6 mice.

Objective We investigated the prevalence of abnormal thyroid function and depression in centrally obese participants, and to analyze the relationship of thyroid hormones and depression with components of central obesity. Methods We randomly selected 858 centrally obese participants and 500 non-obese controls in this study. For all participants, we measured serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), body mass index (BMI), waist–hip ratio (WHR), fasting blood glucose and insulin, homeostasis model assessment of insulin resistance (HOMA-IR), lipid concentrations, and blood pressure. Depression was assessed using the Center for Epidemiological Studies-Depression (CES-D) scale. Results Centrally obese participants had a higher prevalence of hypothyroidism and depression than non-obese controls. Serum FT4 levels negatively correlated with BMI and serum TSH levels and positively correlated with BMI, WHR, total triglycerides (TG), total cholesterol (TC), and low density lipoprotein cholesterol (LDL-C). After excluding participants with hypothyroidism and hyperthyroidism, serum FT4 levels showed negative correlation and serum TSH levels showed positive correlation with BMI in the remaining centrally obese participants. CES-D scores positively correlated with BMI. Conclusion We found high prevalences of hypothyroidism and depression among centrally obese participants. FT4 and TSH are important in weight regulation. Depression positively correlated with obesity.

GLP-1 analogs have been widely used to treat patients with type 2 diabetes in recent years and studies have found that GLP-1 analogs have multiple organ benefits. However, the role of GLP-1 analogs in diabetic retinopathy (DR), a common complication of diabetes mellitus (DM), remains controversial. Retinal ganglion cells (RGCs) are the only afferent neurons responsible for transmitting visual information to the visual center and are vulnerable in the early stage of DR. Protection of RGC is vital for visual function. The incretin glucagon-like peptide-1 (GLP-1), which is secreted by L-cells after food ingestion, could lower blood glucose level through stimulating the release of insulin. In the present study, we evaluated the effects of GLP-1 analog on RGCs both in vitro and in vivo. We established diabetic rat models in vivo and applied an RGC-5 cell line in vitro. The results showed that in high glucose conditions, GLP-1 analog alleviated the damage of RGCs. In addition, GLP-1 analog prevented mitophagy through the PINK1/Parkin pathway. Here we demonstrated the neuroprotective effect of GLP-1 analog, which may be beneficial for retinal function, and we further elucidated a novel mechanism in GLP-1 analog-regulated protection of the retina. These findings may expand the multi-organ benefits of GLP-1 analogs and provide new insights for the prevention of DR.