Sha Sha1,2,3, Xiaoming Liu1,2,3, Ruxing Zhao1,2,3, Li Qing1,2,3, Qin He1,2,3, Lei Sun4,5,6, Li Chen7,8,9. 1. Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, Shandong, China. 2. Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, Shandong, China. 3. Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province medicine& health, Jinan, Shandong, China. 4. Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, Shandong, China. 13969193236@163.com. 5. Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, Shandong, China. 13969193236@163.com. 6. Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province medicine& health, Jinan, Shandong, China. 13969193236@163.com. 7. Department of Endocrinology, Qilu Hospital of Shandong University, Jinan, Shandong, China. chenli3@medmail.com.cn. 8. Institute of Endocrine and Metabolic Diseases of Shandong University, Jinan, Shandong, China. chenli3@medmail.com.cn. 9. Key Laboratory of Endocrine and Metabolic Diseases, Shandong Province medicine& health, Jinan, Shandong, China. chenli3@medmail.com.cn.
Abstract
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.
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 obesemice 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.