Quercetin ameliorates hepatic fat accumulation in high-fat diet-induced obese mice via PPARs

As a natural pigment in food, quercetin possesses multiple biological activities and plays a crucial role in regulating metabolic syndrome. Herein, we aim to explore the potential mechanism of quercetin to ameliorate hepatic fat accumulation. In vivo experiments showed that quercetin significantly relieved inflammation response by decreasing the serum TNF-alpha and IL-6 levels and also improved high-fat diet-induced hepatic steatosis without other organ injuries. Quercetin can effectively reduce lipid aggregation and down-regulate the protein expression of PCK1 in HepG2 cells induced by oleic acid and palmitic acid, indicating that inhibiting gluconeogenesis leads to hepatic fat accumulation reduction. Furthermore, molecular docking results suggested that quercetin can bind to both PPAR alpha and PPAR gamma, with an even more potent binding affinity than indeglitazar, a pan-agonist of PPARs. In conclusion, quercetin may regulate gluconeogenesis to ameliorate hepatic fat accumulation via targeting PPAR alpha/gamma.

Automated summary

As a natural pigment in food, quercetin possesses multiple biological activities and plays a crucial role in regulating metabolic syndrome. In this study, the researchers explored the potential mechanism of quercetin in ameliorating hepatic fat accumulation. The results showed that quercetin could relieve inflammation response, improve high-fat diet-induced hepatic steatosis, and inhibit gluconeogenesis, leading to reduction in hepatic fat accumulation.