Effect of fructose on the phosphorylation of AMP-activated protein kinase and acetyl-CoA carboxylase in HepG2 cells stimulated with placental lactogen.

Abstract

BACKGROUND High fructose intake induces disruption of lipid metabolism via AMP-activated protein kinase (AMPK) signaling in the liver and peripheral tissues. Maternal lipid metabolism is physiologically altered by the activity of pregnancy hormones such as human placental lactogen (PL). To elucidate the influence of high fructose intake on hepatic lipid metabolism during pregnancy, we examined the effects of fructose on lipid metabolism via the AMPK pathway in hepatocytes stimulated with PL. METHODS Human hepatoma cells (HepG2) were treated with D(-)-fructose in the presence or absence of PL. Intracellular lipid contents were measured. The total and phosphorylated protein content of AMPK and acetyl-CoA carboxylase (ACC) was quantified by Western blotting. RESULTS The intracellular triacylglycerol level in fructose-treated HepG2 cells decreased significantly compared with that in untreated cells in the presence, but not absence, of PL. AMPK and ACC phosphorylation increased significantly and concentration-dependently in fructose-treated HepG2 cells in the presence of PL. CONCLUSION Our results suggest that fructose treatment reduces triacylglycerol levels via AMPK/ACC signaling in PL-stimulated hepatocytes. These findings suggest that high fructose intake during pregnancy might impair lipid metabolism in the maternal liver.