The incidence of
obesity has increased significantly on account of the alterations of living habits, especially changes in eating habits. In this study, we investigated the effect of
octacosanol on
lipid lowering and its molecular mechanism. High-fat diet (HFD)-induced
obesity mouse model was used in the study. Thirty C57BL/6J mice were divided into control, HFD, and HFD+Oct groups randomly, and every group included ten mice. The mice of HFD+Oct group were intragastrically administrated 100 mg/kg/day of
octacosanol. After 10 weeks for treatment, our results indicated that
octacosanol supplementation decreased the body, liver, and adipose tissues weight of HFD mice; levels of TC, TG, and
LDL-c were reduced in the plasma of HFD mice; and level of HDL-c were increased. H&E staining indicated that
octacosanol supplementation reduces the size of fat droplets of hepatic tissues and adipose cells comparing with the HFD group. Gene chip analysis found that
octacosanol regulated 72 genes involved in lipid metabolism in the tissues of liver comparing to the HFD group. IPA pathway network analysis indicated that
PPAR and AMPK may play a pivotal role in the
lipid-lowering function of
octacosanol. Real-time quantitative PCR and Western blot showed that the
octacosanol supplementation caused change of expression levels of AMPK, PPARs, FASN, ACC,
SREBP-1c, and
SIRT1, which were closely related to lipid metabolism. Taken together, our results suggest that
octacosanol supplementation exerts a
lipid-decreasing effect in the HFD-fed mice through modulating the lipid metabolism-related signal pathway.