Esteatose hepática: relação com a síndrome metabólica e efeito indutor de dietas padrão utilizadas em experimentação animal

Abstract

The hepatic steatosis is an accumulation of triglycerides in the cytoplasm of the hepatocytes at a level which affects 5 to 10% of the weight of the liver. This entity is part of series of changes that characterize the disease of non-alcoholic fatty liver, which covers, too, changes like non-alcoholic esteatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma. Its etiology, despite not being fully elucidated, shows strong correlation with insulin resistance, and, currently, considered the hepatic manifestation of the metabolic syndrome. This fatty infiltration is a typical response to long-term exposure to harmful stimuli, including hypoxia, toxins, systemic inflammation, malignancies, nutritional deficiencies, starvation and various metabolic disorders. However, despite having been considered for a long time as a benign entity, it is known that the synergistic combination with other factors such as oxidative stress, can trigger reactions in inflammatory cascade, leading to the evolution of the disease. In studies with experimental animals, dietary changes can induce the framework of steatohepatitis, but on previous work done by our group, the onset of disease in groups of animals fed on standard diets, free of changes in its composition original, was observed. Aiming to contribute to the discussion of the problem, this thesis presents two articles: a literature review with the main pathophysiological mechanisms with the advent of steatosis and its relationship with metabolic syndrome, the second article refers to an experimental study with rats newly weaned, who received two kinds of diet: a chow diet Nuvilab and a purified diet proposed by the American Institute of Nutrition, AIN-93. Under the experimental conditions established, the animals that consumed the AIN-93 diet had 90.5% of cases of steatosis, 42.9% in the group subjected to diet AIN-93 G and 47.6% in the group subjected to diet AIN-93 M, observed by histological analysis. This finding shows that despite the changes in its composition to the earlier version, AIN-76A, particularly in its content as sucrose, choline and the amino acid methionine, the problem persists, suggesting that the AIN-93 diet still does not represent the formulation more appropriate for feed for laboratory rodents, especially in the growing phase.