Oat β-glucan inhibits adipogenesis and hepatic steatosis in high fat diet-induced hyperlipidemic mice via AMPK signaling

To evaluate the lowering-lipid effect of oat beta-glucan (O beta G) and its molecular mechanism, high-fat diet (HFD)-induced hyperlipidemic mouse model and oleic acid-induced lipid accumulation model of HepG2 cells were used in this study. O beta G obviously reduced HFD-induced the gain of body weight and epididymal fat pad, and inhibited hepatic adipocyte hyperplasia. These effects were associated with the down-regulation of FAS and SREBP-1, up-regulation of PPAR alpha and particularly the activation of AMP-activated protein kinase (AMPK) signaling in both liver and fat tissues. In the oleic acid-induced HepG2 cells, O beta G partly suppressed lipogenesis and activated AMPK. O beta G inhibited lipid metabolism-related protein expressions such as FAS, SREBP-1, CPT-1, PPAR alpha and activating ACC, which are the downstream targets of AMPK. Taken together, our results suggest that administration of O beta G exerts lipid-lowering effect in HFD mice via AMPK signal pathway, which provide novel application for the prevention and treatment of hyperlipidemia.