Objective:We established a HepG2 hepatic steatosis model to observe whether liraglutide improves lipid metabolism in HepG2 liver cells,and discuss the related mechanisms. Methods:Sodium palmitate was performed to induce HepG2 steatosis model,and liraglutide intervention was given. Oil Red O staining was performed to determine the establishment of HepG2 hepatic steatosis model. Key enzyme of lipid synthesis and degradation as well as the activation of PI3K signaling pathway in HepG2 liver cells were detected by Western blotting assay. To observe the effect of PI3K signaling pathway in sodium palmitate induced HepG2 hepatic steatosis,HepG2 liver cells was pretreated with PI3K signaling pathway inhibitor. Results:Oil Red O staining showed that the model was successfully established. Western blotting assay showed that sodium palmitate significantly increased the expression of sterol regulatory element-binding protein1c(SREBP1c)and fatty acid synthase(FAS)protein levels in HepG2 liver cells,and decreased adipose triglyceride lipase (ATGL)protein levels(P < 0.01); sodium palmitate activated PI3K signaling pathway in HepG2 liver cells. Compared with sodium palmitate,liraglutide significantly decreased the expression of SREBP1c and FAS protein levels in HepG2 liver cells,and increased ATGL protein levels; liraglutide inhibited PI3K signaling pathway in HepG2 liver cells. After blocking PI3K signaling pathway,sodium palmitate-induced steatosis of HepG2 liver cells was significantly reduced (P < 0.01). Conclusion:By regulating PI3K signaling pathway in HepG2 liver cells,liraglutide improves lipid metabolism in HepG2 liver cells.