| Objective To investigate the effects of adiponectin and its receptors on the pathogenesis of non-alcoholic fatty liver disease (NAFLD) rats.Methods Non-alcoholic fatty liver disease (NAFLD) model of rat was established by fat-rich diet (Group F). Control group (Group C) was fed with common diet. There were 18 male SD rats for each group. All rats were killed at the end of the 28th week. Serum fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were measured. Enzyme-linked immunosorbenty (ELISA) was used to measure serum adiponectin and fasting insulin (FINS) concentration. The expression of adiponectin, AdipoR1 and AdipoR2 in liver were detected with immunohistochemiscal methods.Results 1. Compared with group C, weight of the rats (P<0.05), the wet liver weight and liver index (P<0.01) were significantly higher in group F. 2. Compared with group C, serum adionectin level of group F decreased (P<0.05), while TC (P<0.05), HDL-C (P<0.05), TG, LDL-C, FINS and insulin resistance index (IRI) (P<0.01) increased. There was no difference of FBG in two groups. 3. The hepatocytes in group F presented modest to severe big bubble steatosis. There were inflammation and fibrosis in the liver of group F. The quantitive evaluation of steatosis, hepatits and fibrosis were 4.00±0.00, 2.65±0.33, 3.36±0.51 in group F, and 0.76±0.12, 0.32±0.19, 0.12±0.23 in group C separately. There were significant difference between two groups (all P<0.01). 4. Expression of adiponectin was mainly located in endothelial cells of hepatic sinusoid and hepatic portal system. The expression level of adiponectin was 1.46±0.68 vs. 2.17±1.14 in group F and group C. The expression of adiponectin in group F decreased significantly (P<0.05). Expression of AdipoR1 and AdipoR2 were both located in the cytoplasm of hepatic cells. Expression of AdipoR2 decreased in group F compared with group C (3.21±0.45 vs. 5.63±0.27, P<0.01). Expression of AdipoR1 showed no difference between two groups (4.25±1.27 vs. 3.83±1.79, P>0.05).Conclusion 1. NAFLD model rats can be successfully established by fat-rich diet. 2. The decreased concentration of serum adiponection may be concerned with lipid metabolism disorder and insulin resistance.The decreased serum adiponection level and expression of adiponectin and AdipoR2 in liver may play a role in the pathogenesis of NAFLD. |
