Abstract: AIM: To observe the effect of atorvastatin on such adipokines as adiponectin, visfatin and resistin in rats with nonalcoholic fatty liver disease induced by high fat diet.METHODS: The NAFLD model was induced by 10 weeks of high fat diet, then they were intragastrically administrated with atorvastatin. The levels of hepatic TG and CHOL in NAFLD rats were detected by biochemical test. The hepatic steatosis and inflammation were observed with HE staining, the NAFLD activity score(NAS) was counted. The levels of hepatic adiponectin, visfatin and resistin were detected by EL-ISA, the hepatic mRNA expression levels of adiponectin, visfatin and resistin were detected by Realtime PCR.RESULTS: The NAS and levels of hepatic TG and CHOL in model rats were significantly higher than those of normal group (P<0.01), the levels of serum adiponectin and hepatic mRNA expression in NAFLD rats were significantly decreased compared with the normal group (P<0.01), while the levels of visfatin , resistin and their mRNA expression were significantly increased compared with the normal group (P<0.01). After intervention with atorvastatin, the pathology of liver tissue improved, the levels of hepatic TG, CHOL were significantly lower than those of model group (P<0.05), the levels of serum adiponectin and hepatic mRNA expression in NAFLD rats liver were increased compared with the modle group (P<0.05), while the levels of serum visfatin, resistin and hepatic mRNA expression were decreased compared with the model group (P<0.05).CONCLUSION: Disorders of secretion of such inflammatory factors as adiponectin, visfatin and resistin emerge in NAFLD induced by high fat diet. With reducing the deposition of lipids in the liver, raising the expression of adiponectin, inhibiting the overexpression of visfatin and resistin, atorvastatin may inhibit inflammation reaction of hepatocytes , prevent NAFLD progress.

Key words: atorvastatin, nonalcoholic fatty liver disease, adiponectin, visfatin, resistin