Glucagon-Like Skin-1’s Effect on Islet β Cells in High Glucose via AMPK/mTOR Pathway

Abstract

This study investigated whether GLP-1 affects islet β cells in high glucose and the possible mechanism. INS-1 cells are separated into group A (treated with 5.6 mmol/L glucose), group B (group A+100 nmo1/L liraglutide), group C (cells were cultured in 16.7 mmol/L glucose) and group D (group C+100 nmo1/L liraglutide) followed by analysis of cell activity by CCK-8, apoptosis by Hoechst staining, INS level by ELISA, AMPK/mTOR signaling protein level by immunoblotting and RT-PCR. Compared with group A, cell proliferation was significantly increased in group B (P <0.05) and decreased in group C which had lower cell proliferation than group D (P <0.05). However, opposite results were obtained regarding cell apoptosis in four groups (P <0.05); group B showed higher INS level (145.36±8.55 pg/ml) and group C had lower level (80.14±5.36 pg/ml) than group A (105.23±7.78 pg/ml) (P <0.05). Meanwhile, AMPK and p-AMPK levels were significantly lower in group B and higher in group C than group A (P <0.05) with lower level in group D than group C (P <0.05). Whereas, opposite expression profile of p-mTOR and mTOR was found in these groups (P <0.05). High glucose inhibits INS-1 cell proliferation and promotes apoptosis. GLP-1 analogue inhibits INS-1 cell apoptosis in high glucose and accelerate proliferation possibly via regulation of AMPK/mTOR signaling pathway.