Authors: Zhenhua Liu, Lanting Xu, Meimei Xing, Xiaojie Xu, Jinfeng Wei, Jinmei Wang, Wenyi Kang

Journal: Biomedicine & Pharmacotherapy

May 2020, Volume 125, 109952

https://doi.org/10.1016/j.biopha.2020.109952

中文简介：http://syj.henu.edu.cn/info/1061/1077.htm

·Trelagliptin succinate increased glucose uptake in fat cells and Insulin-resistant 3T3-L1 adipocytes.

·Trelagliptin succinate increased the content of GLUT4 in the outer membrane of fat cells.

·Trelagliptin succinate decreased the content of extracellular FFA and Resistin.

·Trelagliptin succinate promoted the expression of PI-3K, P-AKT, P-IRS-1, GLUT4 in 3T3-L1 insulin-resistant adipocytes.

Trelagliptin inhibits the enzyme dipeptidyl-4 (DPP-4) to treat type 2 diabetes and it may possess the potential to improve insulin resistance. However, the molecular mechanism is not known. In this study, the effect of trelagliptin succinate in improving insulin resistance was investigated. The differentiation system of 3T3-L1 mouse preadipocytes was used to determine the content of adipokines and the content of GLUT4 in the outer membrane. The expression of AKT, P-AKT, IRS-1 and P-IRS-1 in differentiated 3T3-L1 adipocytes was determined by western blotting. Our results demonstrated that trelagliptin succinate increased the expression of AKT, P-AKT, IRS-1 and P-IRS-1 in the PI-3K/AKT insulin signaling pathway. These events promote the trans-membrane function of GLUT4 and concomitant glucose intake in adipocytes. In addition, the secretion of free fatty acids and resistin were decreased. In conclusion, our study suggested that trelagliptin succinate improved insulin resistance in adipocytes via regulation of PI-3K/AKT/GLUT4 insulin signaling pathway.