Modelo experimental de obesidade em ratos, por dieta enriquecida com sacarose: ênfase na patogenia da doença hepática gordurosa não alcoólica

Abstract

Introduction: Obesity is currently an epidemic disease caused in part by dietary consumption of saturated fats and simple sugars and a sedentary lifestyle; it can lead to non-alcoholic fatty liver disease (NAFLD) whose prevalence in obese patients with diabetes mellitus type 2 is of approximately 70%. Many aspects of NAFLD are as yet unknown. The aim of the study was to develop an experimental model of NAFLD to analyse pathogenic and pathophysiological changes related to this entity. Method: Thirty wistar rats were fed an added dietary sucrose (experimental group - GE); 30 received standard diet (control group - GC). Six rats from each group were sacrificed on the 5th, 10th, 20th and 30th weeks. At that occasion, anthropometric, biochemical, metabolic and hormonal parameters as well as oxidative stress markers, antioxidant enzymes and liver histology were evaluated. After obesity was established, 12 animals from each group (GEex and GCex) were submitted to physical training for five weeks and the various parameters were evaluated. Results: Glucose, VLDL-cholesterol and triglycerides levels were higher in the GE at 30 weeks; insulin and leptin levels were constantly higher in the GE. There was a positive correlation between an increase in BMI and serum leptin levels. The antioxidant enzymes superoxide dismutase and catalase were lower in the GE at 30 weeks. Steatosis and hepatocellular ballooning as well as malondialdehyde levels were observed only in the GE. Hepatic expression of the Ob-R receptor of leptin was positive in both groups, while leptin expression was more intense in the EG. HDL cholesterol levels were higher and hepatic lipid peroxidation lower in rats submitted to physical exercises. Conclusion: Diet rich in simple carbohydrates induced obesity that contributes to the development of NAFLD. Physical training reduced levels of hepatic lipid peroxidation.