Genistein Ameliorates Fat Accumulation Through AMPK Activation in Fatty Acid-Induced BRL Cells

Abstract

Genstein is the most abundant phytoestrogen in soybean that was reported to play positive roles in menopausal syndrome and metabolic syndrome. In the present study, we investigated the effects and potential mechanisms of genistein against progression of nonalcoholic fatty liver disease (NAFLD) in BRL cells treated with fatty acid mixture (oleate/palmitate, 2:1 ratio). Our data demonstrated that genistein remarkably improved fatty acid mixture-induced hepatocelluler fat accumulation, inhibited upregulation of genes expression related to fatty acid synthesis, and derepressed those associated with fatty acid oxidation. In addition, the results displayed that genistein promoted the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) suppressed by fatty acid, which were significantly weakened by compound C, an AMPK inhibitor. Taken all together, genistein is capable to ameliorate fat accumulation through regulation of fatty acid metabolism mediated by AMPK activation in BRL cells. Further investigations are needed to verify the protective effects of genistein on NAFLD model in in vivo animal study or in vitro human cell lines along with absorption, distribution, metabolism, and excretion studies of genistein.

Practical application: Genistein is able to ameliorate fat accumulation through regulation of fatty acid metabolism mediated by AMPK activation in vitro.

Keywords: adenosine monophosphate-activated protein kinase; fatty acid metabolism; genistein; nonalcoholic fatty liver disease.