Morphological disorder progression in rat high-fat, high-carbohydrate diet induced metabolic syndrome

Abstract

Introduction: High-fat-carbohydrate intake correlates with the epidemic rise in obesity and metabolic syndrome and related events. Additionally, the prevalence of hepatic steatosis and cirrhosis was reported to be high among patients with obesity and type 2 diabetes. The aim of our work was to study the liver and mesenteric aipose tissue morphology in male rats with metabolic syndrome induced by high-fat, high-carbohydrate diet (HFCD). Material And Methods: Male Wistar rats (n=10) were fed HFCD for 16 weeks. Control rats (n=10) were fed a normal diet for the same period of time. Metabolic control was determined by measuring body weight gain, BMI, adiposity, plasma biochemical parameter. Histopathological study was performed on the visceral mesenteric adipose tissue and liver (glycogen and lipid content) using routine staining with hematoxylin-eosin and histochemical PAS reaction and Sudan III staining. Results: After 16 weeks HFCD increased body weight, BMI, adiposity, associated to decreased HDL cholesterol. Mesenteric adipose tissue was with larger adipocytes in comparison with the controls. Liver steatosis was also observed in the HFCD group, which was associated with an increase in glycogen and lipid storage.Conclusion: Nutritional stress such as that caused by HFCD promotes oxidative stress as evident by increased lipid peroxidation products and de novo lipogenesis which contributed to fat accumulation in the adipose tissue and liver and the development of non-alcholic liver disorders.