Quercetin improves insulin resistance and hepatic lipid accumulation in vitro in a NAFLD cell model.

Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver diseases in the absence of significant alcohol consumption. The aim of this study was to investigate the effect of quercetin on insulin resistance and lipid metabolic abnormalities in free fatty acid (FFA)- and insulin-induced HepG2 cell model of NAFLD, and to determine the possible underlying mechanism. Quercetin markedly improves hepatic lipid accumulation and decreases the levels of triglyceride (TG). The lipid-lowering effect of quercetin at concentrations between 0.1 and 100 μM demonstrated a dose-dependent pattern. Quercetin was found to enhance tyrosine phosphorylation in the insulin-signaling pathway and to downregulate the expression levels of the sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) in quercetin-treated groups, compared to the control group. These results demonstrated that quercetin was able to improve insulin resistance and hepatic lipid accumulation by suppressing two lipogenesis gene expression levels of SREBP-1c and FAS. As a result, quercetin has the therapeutic potential for preventing or treating NAFLD and IR-related metabolic disorders.