| Literature DB >> 26254015 |
Jinmi Lee1, Seok-Woo Hong1, Se Eun Park2, Eun-Jung Rhee2, Cheol-Young Park2, Ki-Won Oh2, Sung-Woo Park2, Won-Young Lee3.
Abstract
ANGPTL8 is a liver-derived secretory protein that leads to elevated serum triglyceride and the level of circulating ANGPTL8 is strongly associated with obesity and diabetes. Here we investigated the mechanisms of activation and inhibition of ANGPTL8 expression in hepatocytes. The expression of ANGPTL8 was significantly increased in HepG2 cells exposed to palmitic acid, tunicamycin, or T0901317, and was reversed in cells treated with AICAR. Palmitic acid, tunicamycin, and T0901317 increased LXRα and SREBP-1c mRNA expression. The inhibitory effect of AICAR on the expression of T0901317-induced ANGPTL8 was most strongly evident in cells that were transfected with SREBP-1 siRNA. AICAR increased phosphorylation of PPARα and the effect of AICAR was not observed in cells treated with PPARα inhibitor. Metformin had a similar effect on ANGPTL8 expression to that of AICAR. These data suggest that AMPK can suppress the expression of LXR/SREBP-1 signal-induced ANGPTL8 in HepG2 cells.Entities:
Keywords: AMPK; ANGPTL8; Hepatocytes; LXR; PPAR alpha; SREBP-1
Mesh：
Substances：
Year: 2015 PMID： 26254015 DOI： 10.1016/j.mce.2015.07.031
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN： 0303-7207 Impact factor: 4.102