Exploring the non‐alcoholic fatty liver disease pathogenesis mechanisms in high fat and high fructose diet fed rat (649.3)

Abstract

The prevalence of fatty liver in western country is 30%. Western diet (high fat and/or high fructose) induce chronic and low grade inflammation in adipose tissue that initiate the first step of many complications such as cardiovascular disease, diabetes and fatty liver disease. However, high fat diet trigger obesity and high fructose diet perform a normal body weight, but all result in NAFLD. Therefore, it is important to elucidate the different mechanism of fatty liver pathogenesis in high fat and high fructose diet fed animal model(s).The SD rats were fed with high fat diet (HF, 45 calorie from fat) and high fructose diet (HR, 60 calorie from fructose) for 12 weeks. We found that both two western diets led to hepatic steatosis, hyperglycemia, hyperlipidemia, hyperinsulinemia and insulin resistance. Triglyceride and cholesterol were accumulated in liver tissue, accompanied with plasma ALT/AST elevation. Interestingly, HR induced higher hepatic ROS level, which implies the different hepatic stress, and the key NAFLD progression regulator compared with HF fed rats. In the conclusion, we suggested ROS, the distinct NAFLD mediator in HR, not a like with HF rats, many additionally promote the severe NAFLD progression.