Lycopene prevents lipid accumulation in hepatocytes by stimulating PPARα and improving mitochondrial function
Jia Wang, Tonghui Geng, Qianhui Zou, Ningru Yang, Weiyang Zhao, Yitong Li, Xintong Tan, Tian Yuan, Xuebo Liu, Zhigang Liu
Abstract
The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased over the decades. Lycopene (LYC), a major carotenoid present in tomato, has been previously demonstrated to possess liver-protecting and lipid-lowering bioactivities. However, the underlying mechanism of how LYC impact on the lipid metabolism in the liver is elusive. Here, we found that LYC significantly suppressed lipid accumulation in palmitate- treated HepG2 hepatocytes cell line by stimulating PPARα expression and enhanced lipolysis consequently. It has also been revealed that LYC prevented palmitate-induced mitochondrial dysfunction by improving mitochondrial complex expression and activating mitochondrial biogenesis pathway AMPK/SIRT1/PGC1α. Moreover, in line with in vitro study, LYC treatment significantly suppressed lipid accumulation and enhanced PPARα expression in western diet-feeding mice liver. LYC also enhanced the expressions of mitochondrial complexes and antioxidant related enzymes HO-1/NQO1. In conclusion, the mediating effects of LYC on mitochondrial function and PPARα signaling might play pivotal roles in its beneficial effects on NAFLD.