95 RUTIN ATTENUATES NON-ALCOHOLIC STEATOHEPATITIS IN HIGH CARBOHYDRATE-HIGH FAT DIET-FED RATS

Abstract

Background and Aims: Non-alcoholic fatty liver disease (NAFLD) is frequently associated with the signs of metabolic syndrome, especially obesity, dyslipidaemia and insulin resistance. Metabolic syndrome and NAFLD are associated with cardiac hypertrophy, ventricular dysfunction and endothelial dysfunction. Rutin, a glycoside of the flavonol quercetin, is found in onions, apples, tea and red wine. In this study, we characterised the hepatoprotective and cardioprotective effects of rutin (1.6 g/kg food) in a model of diet-induced metabolic syndrome, non-alcoholic steatohepatitis and cardiovascular remodelling (Panchal et al.2010). Methods: 8–9 weeks old male Wistar rats were divided into 2 diet groups (n = 36 each) with corn starch (CS) or high carbohydratehigh fat (HCHF) diets (Panchal et al. 2010). 12 rats from each group were used after 8 weeks, 12 rats from each group continued on the same diet for 16 weeks without interventions and 12 rats from each group were treated with rutin (1.6 g/kg food) in the diet for the last 8 weeks. Metabolic profile, structure and function of liver and heart were assessed at the end of the protocol (Panchal et al.2010). Western blot analysis was used to study the expression of caspase-3, Erk and Hsp70 in liver. Results: HCHF-fed rats showed the signs of metabolic syndrome including central obesity, dyslipidaemia, impaired glucose tolerance and hypertension, cardiovascular remodelling and endothelial dysfunction together with steatosis, inflammation and fibrosis in the liver along with increased plasma activities of ALT, AST, ALP and LDH and increased expression of caspase-3, Hsp70 and Erk. Rutin treatment in HCHF-fed rats improved or reversed these changes. Conclusions: Supplementation of a high carbohydrate-high fat diet with rutin effectively attenuated or reversed the signs of metabolic syndrome, cardiovascular remodelling and non-alcoholic steato-hepatitis in this rat model of diet-induced obesity and liver dysfunction.