Author/Authors :
jing Yin، Jia نويسنده The Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, China , , bo Li، Yan نويسنده The Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, China , , ming Cao، Ming نويسنده The Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, China , , Wang، Yang نويسنده ,
Abstract :
Type 2 diabetes mellitus (T2D) is a metabolic disease characterized by dysfunction of pancreatic beta cell and insulin resistance. Liraglutide, which has many special anti-diabetes biological effects, is found to inhibit beta cell death and ameliorate endoplasmic reticulum stress (ERs) induced by free fatty acid (FFA). Macroautophagy (hereafter referred to as autophagy) altered by FFA is also associated with the dysfunction or death of pancreatic beta cells. We aim at proving that Liraglutide improves the survival of INS-1 cells by promoting autophagy. Cell survival was assessed by CCK8 assay. The percentage of apoptotic cells was determined by flow cytometric assay after Annexin V-FITC/PI staining. Expression of LC3 was detected by western blotting. MDC staining and transmission electron microscopy (TEM) were used in the measurement of autophagy. Apoptosis induced by PA in INS-1 cells was significantly resolved after Liraglutide treatment. Simultaneously, autophagy was enhanced with the treatment of PA and Liraglutide. Conclusions: Liraglutide appears to protect INS-1 cells from apoptosis FFA-induced by promoting autophagy. These findings provide a novel role for GLP-1 analogue in preventing or treating with T2D.
