The effect of rosiglitazone on non-alcoholic fatty liver in experimental rats

ABSTRACT

Objective To investigate the effect of rosiglitazone on non-alcoholic fatty liver (NA and to explore the relationship between insulin resistance and NAFL. Methods Animal model of NAFL was established by feeding Sprague-Dawley rats a high-fat diet for 8 weeks. The model rats were then randomized into rosiglitazone-treated and untreated groups. The animals were sacrificed after being treated with rosiglitazone or vehicle for 4 weeks. The histological changes of liver were examined, and liver function, fasting plasma glucose, fasting serum insulin, serum lipid profile, leptin, and adiponectin were measured. Results As compared with untreated group, hepatic steatosis and liver function were significantly improved in rosiglitazone-treated group. Alanine aminotransferase (ALT) was 54±19 U/L vs 101±24 U/L, aspartic acid aminotransferase (AST) 151±37 U/L vs 198±48 U/L, and alkaline phosphatase (ALP) 87±16 U/L vs 115±39 U/L, respectively (P<0.01). Serum adiponectin level was higher, and serum leptin level and insulin resistance index (HOMA-IR) were lower in rosiglitazone-treated group than in untreated group. HOMA-IR was 6.9±1.8 vs 12.0±1.2 (P<0.01). Serum triglyceride, total cholesterol and low density lipoprotein-cholesterol level were significantly decreased in rosiglitazone-treated group as compared with untreated group (P<0.01). Conclusions Insulin resistance might play important role in the pathogenesis of NAFL. Rosiglitazone effectively reverses NAFL in animal model.