Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice.

ABSTRACT: Previous findings supported that fetuin B, a new hepatokine, may be involved in the development of hepatic steatosis, but the mechanism is still unknown. This study aims to investigate the role of fetuin B in hepatic steatosis in C57BL/6 mice and HepG2 cells. 1) We found that the administration of recombinant fetuin B aggravated hepatic lipid accumulation caused by free fatty acids (FFAs) or high fat diet, in vivo and in vitro. It lowered the phosphorylated AMPK levels and activated the LXR-SREBP1c pathway, accompanied by the downregulation of fatty acid oxidation and upregulation of lipogenesis. Furthermore, in HepG2 cells exposed to recombinant fetuin B and FFAs, the AMPK agonist depressed the LXR-SREBP1c pathway and alleviated lipid accumulation. The knockdown of LXR prote

SUBMITTER: Zhou W 

PROVIDER: S-EPMC6456555 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature