Abstract: Abstract：The purposes of this study were to elucidate the underlying mechanism responsible for the impact of fibroblast growth factor 21 （FGF21） on AMPK phosphorylation regulatory factors, and to clarify the effect of FGF21 on lipid droplet metabolism mediated by high NEFA in mouse hepatocytes. The AML12 mouse hepatocytes were received the treatment of NEFA addition and （or） FGF21 gene silencing; after that, the mRNA expression levels of FGF21, hepatokinase B1 （LKB1）, transforming growth factor β-activated kinase 1 （TAK1）, and calcium/calmodulin-dependent protein kinase kinase（CaMKK） of the mouse hepatocytes were assessed by using fluorescence quantitative PCR assay; the level of hepatic lipid deposition was detected by oil red O staining. The results showed that silencing of FGF21 gene significantly （P<; 0.05） decreased the mRNA expression level of LKB1, but had no significant effect on the mRNA expression level of TAK1 and CaMKK （P>; 0.05）. Furthermore, the level of lipid deposition in hepatocytes was significantly （P<; 0.05） elevated after silencing of FGF21 gene under high NEFA. In conclusion, FGF 21 may reduce the lipid deposition in mouse hepatocytes under high NEFA by activating AMPK signaling pathway via inducing LKB1.

Key words: AML12 mouse hepatocytes, FGF21, LKB1, AMPK, lipid metabolism