Liraglutide reduces fatty degeneration in hepatic cells via the AMPK/SREBP1 pathway.

Recent studies have suggested that liraglutide could have a potential function in improving non-alcoholic fatty liver disease (NAFLD); however, the underlying molecular mechanism remains unclear. The aim of the present study was to investigate the role of the AMP-activated protein kinase (AMPK)/sterol regulatory element binding protein 1 (SREBP1) pathway in mediating the effect of liraglutide in reducing fatty degeneration in an NAFLD model. To resemble the NAFLD condition , L-02 cells were treated with 0.5 mM free fatty acids (FFAs) for 24 h. Liraglutide could affect the expression of AMPKα1, phosphorylated AMPKα1 and SREBP1 in a dose-dependent manner in FFA-exposed L-02 cells, as demonstrated by western blot analysis. The intracellular lipid accumulation was significantly decreased, as shown by oil red O staining. A significant decrease in the content of triglyceride and total cholesterol was observed when the FFA-exposed L-02 cells were incubated with liraglutide. In addition, the increased expression of liver-type fatty acid-binding protein in FFA-exposed L-02 cells was suppressed by liraglutide. These effects were reversed by compound C, an AMPK inhibitor. In conclusion, this study has demonstrated that liraglutide can reduce fatty degeneration induced by FFAs in hepatocytes, and this effect may be partially mediated by the AMPK/SREBP1 pathway.