The aim of this study was to investigate the antiobesity and antihyperlipidaemic effects of
emodin on high-fat diet (HFD)-induced obese rats, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. After being fed HFD for two weeks, Wistar rats were dosed orally with
emodin (40 and 80 mg kg(-1)) or
pioglitazone (20 mg kg(-1)), once daily for eight weeks.
Emodin (80 mg kg(-1) per day) displayed similar characteristics to
pioglitazone (20 mg kg(-1) per day) in reducing
body weight gain, plasma
lipid levels as well as coronary artery risk index and atherogenic index of HFD-fed rats.
Emodin also caused dose related reductions in the hepatic
triglyceride and
cholesterol contents and lowered hepatic lipid droplets accumulation in HFD-fed rats.
Emodin and
pioglitazone enhanced the phosphorylation of
AMP-activated protein kinase (AMPK) and its primary downstream targeting
enzyme,
acetyl-CoA carboxylase, up-regulated gene expression of
carnitine palmitoyl
transferase 1, and down-regulated
sterol regulatory element binding protein 1 and
fatty acid synthase protein levels in hepatocytes of HFD-fed rats. Our findings suggest
emodin could attenuate
lipid accumulation by decreasing lipogenesis and increasing mitochondrial
fatty acid β-oxidation mediated by activation of the AMPK signaling pathway.