AMP-activated protein kinase suppresses the expression of LXR/SREBP-1 signaling-induced ANGPTL8 in HepG2 cells

作者：Lee Jinmi; Hong Seok Woo; Park Se Eun; Rhee Eun Jung; Park Cheol Young; Oh Ki Won; Park Sung Woo; Lee Won Young^*

来源：Molecular and Cellular Endocrinology, 2015, 414(C): 148-155.

DOI：10.1016/j.mce.2015.07.031

• ANGPTL8
• LXR
• SREBP-1
• AMPK
• PPAR alpha
• Hepatocytes

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 LXR alpha 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 PPAR alpha and the effect of AICAR was not observed in cells treated with PPAR alpha 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.

• 出版日期2015-10-15
• 单位河北医科大学