Oestrogen promotes lipids transportation through oestrogen receptor alpha in hepatic steatosis of geese in vitro

Evidence has shown that oestrogen suppresses lipids deposition in the liver of mammals. However, the molecular mechanism of oestrogen action in hepatic steatosis of geese liver has yet to be determined. This study aimed to investigate the effect of oestrogen on lipid homeostasis at different states of geese hepatocytes in vitro. The results showed that an in vitro model of hepatic steatosis was induced by 1.5 mM sodium oleate via detecting the viability of hepatocytes and content of lipids. When the normal hepatocytes were administrated with different concentrations of oestrogen (E-2), the expression levels of diacylglycerol acyltransferase 2 (DGAT2), microsomal triglyceride transfer protein (MTTP) and oestrogen receptors (ERs, alpha and beta) were up-regulated only at high concentrations of E-2, whereas the lipid content was not a significant difference. In goose hepatocytes of hepatic steatosis, however, the expression levels of MTTP, apolipoprotein B (apoB) and ER alpha/beta significantly increased at 10(-7) or 10(-6) M E-2. Meanwhile, the lipids content significantly increased at 10(-9) and 10(-8) M E-2 and decreased at 80 mu M E-2. Further heatmap analysis showed that ER alpha was clustered with apoB and MTTP in either normal hepatocytes or that of hepatic steatosis. Taken together, E-2 might bind to ER alpha to up-regulate the expression levels of apoB and MTTP, promoting the transportation of lipids and alleviating lipids overload in hepatic steatosis of geese in vitro.

Automated summary

Evidence suggests that estrogen may up-regulate the expression levels of proteins related to lipid transportation, thereby alleviating lipid overload in hepatic steatosis of geese in vitro.