Lycopene prevents lipid accumulation in hepatocytes by stimulating PPARα and improving mitochondrial function

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.

Keywords

• Lycopene
• Lipid metabolism dysfunction
• Mitochondrial function
• Nonalcoholic fatty liver disease
• PPARα