Luteolin Ameliorates Hepatic Steatosis and Enhances Mitochondrial Biogenesis via AMPK/PGC-1α Pathway in Western Diet-Fed Mice.

Abstract

Luteolin (LU), a natural compound, has diverse bioactivities; it alleviates lipid accumulation by enhancing the oxidation of fatty acids in nonalcoholic fatty liver disease (NAFLD). Mitochondrial dysfunction promotes the development of steatosis in NAFLD. However, few studies have focused on the mechanism by which LU affects mitochondrial function in NAFLD. In the present study, we investigated whether LU could ameliorate hepatic steatosis and affect mitochondrial function in Western diet-fed mice. After LU treatment, the indicators of hepatic function and markers of mitochondrial biogenesis were evaluated. The results showed that LU intervention 1) decreased the levels of serum triglyceride, total cholesterol, alanine aminotransferase, and low-density lipoprotein cholesterol; 2) increased the succinate dehydrogenase activity of mitochondrial enzyme; and 3) increased mitochondrial biogenesis by upregulating the AMPK/PGC-1α pathway. Therefore, LU might have the potential to prevent NAFLD.