Effects of glucagon-like peptide-1 analog liraglutide on the systemic inflammation in high-fat-diet-induced mice.

OBJECTIVE: Metabolic syndrome is a chronic-metabolic disease caused by a variety of factors, including high peripheral blood insulin levels and insulin resistance. It has been reported that GLP-1 could regulate insulin resistance. It is not known whether and how GLP-1 protects from fat-induced inflammation and immune changes. We investigated if GLP-1 alters the populations of fat-induced inflammation and immune cells and the related mechanism. METHODS: We obtained obese C57BL/6J mice by feeding them high-fat food, then treated the obese mice with GLP-1+ high-fat diet (G + Hi), normal chow diet (Nor), or high-fat diet (Hi) (n = 20 for each group) for 8 weeks. The GLP-1 receptor-/- B6 group were fed with HFD for 8 weeks (GLP-1R KO + Hi). In vivo and in vitro experiments were conducted on mice immune cells to investigate the effects of GLP-1 on the changes of the immune components and functions in obesity. RESULTS: We found that GLP-1 could efficiently change the CD4+ T subsets and level of cytokines in high-fat-induced mice by GLP-1 receptor. Further, these changes were correlated with a reduction in fat content and serum lipid level. Interestingly, GLP-1 could enhance the function of Tregs in vitro. CONCLUSION: Our data showed that GLP-1 has an important role in shaping the CD4+ T population in high-fat-diet-induced mice by GLP-1 receptor, possibly providing a new target for the treatment of metabolic syndrome.