Exercício físico de baixa intensidade como estratégia protetora contra a doença hepática gordurosa não alcoólica associada à síndrome metabólica em um modelo murino-dietético

Abstract

Non-alcoholic fatty liver disease (NAFLD) refers to a large spectrum of liver damage resulting from the accumulation of lipids in the liver. There is two types of NAFLD: (1) associated with metabolic syndrome (MetS) and (2) independent of MetS. Clinical guidelines recommend moderate or high intensity exercise as a strategy for the treatment of metabolic dysfunctions, among them the NAFLD. However, such exercise leads to high metabolic and cardiovascular stress. The aim of this thesis was to investigate the hepatic and systemic effects of a low-intensity exercise protocol in the swimming mode in a murine-dietary model of NAFLD associated with MetS. C57B1 / 6 mice consumed high fat diet (58.4% of kilocalories derived from lipids) or standard diet (14% of kilocalories from lipids). After seven weeks of dietary intervention, a low- intensity exercise protocol started for swimming groups. The swimming protocol consisted of 2 sessions of 90 minutes per day, 5 days per week, for 4 weeks. The results indicated that high fat diet established the NAFLD phenotype associated with the metabolic syndrome in C57Bl/6 mice with increased white adipose tissue, glucose intolerance, reduced insulin sensitivity, dyslipidaemia and hepatic steatosis. Low intensity physical exercise reversed all metabolic dysfunctions. The experimental swimming model avoided hepatic steatosis by regulating plasma levels of leptin, reducing CD-36 gene expression and increasing expression of ACC-1 and FAS genes. In addition, low-intensity physical exercise was able to increase the antioxidant activity of catalase and reduce the expression of the pro-inflammatory cytokine IL-6, suggesting a protective role against the progression of NAFLD. Thus, we concluded that low intensity physical exercise is a promising tool for the management of NAFLD associated with MetS because of its ability to reduce hepatic steatosis and to modulate parameters associated with inflammation and redox imbalance, which contribute to the progression of NAFLD.