Vitamin C Inhibits the Nonalcoholic Fatty Liver Induced by High Fat Diet in Mice Regulating PPAR-α Target Gene

OBJECTIVE To explore whether vitamin C could inhibit high-fat diet induced nonalcoholic fatty liver disease (NAFLD) mouse model by regulating PPAR-α target gene. METHODS C57BL/6 mice were divided into control group, NAFLD group and vitamin C group. Each group consisted of 10 mice. The control group was fed with normal diet for 15 weeks; the NAFLD group was fed with high-fat diet for 15 weeks; vitamin C group were fed with high-fat diet and vitamin C for 15 weeks. After 15 weeks of feeding, variables and determinants of NAFLD were examined using metabolic measurements, histology, and gene expression. RESULTS Compared to NAFLD group mice, administration of vitamin C to obese mice reduced body weight gain(P<0.05). Concomitantly, circulating vitamin C concentrations were significantly higher in vitamin C mice than in NAFLD mice(P<0.05). Vitamin C could inhibit hepatic steatosis(P<0.05). Similarly, vitamin C also reduced the mRNA levels of liver inflammation, fibrosis and apoptosis related genes in NAFLD mice(all P<0.05). In addition, serum alanine aminotransferase, aspartate aminotransferase, total cholesterol and low density lipoproteincholesterol levels in vitamin C mice were lower than those in NAFLD mice(all P<0.05). Vitamin C could also increase the mRNA level of PPAR-α-mediated fatty acid β oxidation gene in liver(all P<0.05). CONCLUSION Vitamin C can inhibit weight gain, liver triglyceride accumulation, liver inflammation, fibrosis and apoptosis in NAFLD mice, which may be partly mediated by up regulating PPAR-α target gene expression.