Studies have shown that intestinal microbiota is involved in metabolic endotoxemia-induced by high-fat diet, in adipose tissue inflammation, in the generation of oxidative stress and consequently in the development of metabolic disorders. It has been suggested that the modulation of intestinal microbiota by the use of prebiotics in obese mice can act favorably on the intestinal barrier, with beneficial consequences for associated metabolic disorders. The short-chain fatty acids, products of bacterial fermentation, as for example, butyrate, have been considered a trophic factor for the intestinal mucosa, mainly through the reduction of intestinal permeability by modulating the expression of cell junction proteins, such as ocludinas, claudin and ZO-1. However, these effects were not demonstrated in vivo and little is known about the molecular mechanisms involved in the improvements in metabolic parameters and in inflammatory response promoted by butyrate. Thus, this work aims to study the effect of butyrate on permeability and intestinal and systemic immune response, as well as modification and metabolic profile of mice fed high-fat diet.
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