Abstract

The paper presents analysis of the data of worldwide literature, results of evidence-based experimental and clinical trials on the relationship between dietary habits and intestinal microbiota. The particular attention is paid to the involvement of intestinal dysbiosis and small intestinal bacterial overgrowth syndrome in the pathogenesis of obesity and metabolic syndrome. The arguments in favour of two leading hypotheses have been outlined: hypothesis of metabolic endotoxemia and «storage» hypothesis. The first one considers mechanisms of the effects of lipopolysaccharide Gram-negative intestinal flora, increased permeability of intestinal wall, endocannabinoid system, and intestinal alkaline phosphatase. The «storage» hypothesis takes into account the peculiarities of food polysaccharides’ fermentation, monosaccharides’ absorption, and the role of intestinal microbiota and metabolites of its vital activity (in particular, short-chain fatty acids) in the regulation of lipid metabolism. Particular attention is paid to the treatment: dietary changes, the use of pro- and prebiotics, fecal transplantation. The effects of food components on the intestinal microbiota have been analysed, including the dietary fiber, such as resistant starch and inulin, and fats and proteins. It has been shown that the composition of the intestinal microbiota reflects the dietary habits and composition of the diet. A high-fat diet dramatically increases the intestinal permeability due to a mechanism associated with reduced expression of proteins of epithelial tight junction, including zonulin and occludin. The substantiation has been given to the hypothesis that the intestinal microbiome associated with obesity has an increased ability to receive energy from food («accumulation effect»). Benefits of an antibiotic with a low intestinal absorption (rifaximin) have been analysed. The results of studies supporting the eubiotic properties of rifaximin and its effectiveness at intestinal dysbiosis have been presented.

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