Pathogenetic Role of the Intestinal Microflora in the Obesity Development

Abstract

The purpose of the study was to analyze the sources of modern literature of domestic and foreign researchers on the role of intestinal microbiota in the pathogenesis of obesity. Results and discussion. The number of patients with obesity and associated cardio-metabolic disorders such as arterial hypertension, dyslipidemia, coronary heart disease, type 2 diabetes mellitus is constantly increasing. The increase in the prevalence of obesity and metabolic disorders cannot be attributed solely to changes in the human genome, dietary habits, or reduced levels of physical activity. In addition to the generally recognized reasons, one of the factors affecting the microorganism’s energy homeostasis is the intestinal microbiota. Intestinal microbiota is a collection of bacteria that inhabit the gastrointestinal tract. Intestinal microbiota and its active metabolites are involved in intestinal and hepatic gluconeogenesis, in fat homeostasis, in the synthesis of incretin hormones, and influence on the appetite regulation. Short-chain fatty acids are the most important metabolites of intestinal microbiota. Some bacteria of the Firmicutes, Eubacterium rectale/Roseburia phylum and Faecalibacterium prausnitzii and others produce short-chain fatty acids. Short-chain fatty acids perform a detoxifying function, maintain water and electrolyte balance, and participate in immune response processes by reducing the synthesis of pro-inflammatory interleukins. Intestinal microbiota is also considered as one of the potential sources of metabolic endotoxemia formation. The role of endotoxin in the human body is performed by one of the components of the outer membrane of gram-negative bacteria – lipopolysaccharide. It is constantly present in the blood, and at “physiological” concentrations it maintains the balance of the immune system, and “excessive” concentration of lipopolysaccharide in the blood leads to low-grade inflammation, endothelial dysfunction, and other inflammation-associated conditions. The degree of endotoxemia positively correlates with the severity of negative changes in lipid and carbohydrate metabolism. Also, intestinal microbiota can send signals to the central nervous system through the enteric nervous system or through the afferent fibers of the nervus vagus, both directly and through the release of neurotransmitters into the bloodstream. In turn, when transmitting signals from top to bottom, the autonomic nervous system and the hypothalamus-pituitary-adrenal axis affects intestinal microbiota, probably due to changes in the chemical composition of secretions. Conclusion. Members of intestinal microbiota can inhibit the activity of the enzyme adenosine monophosphate-activated protein kinase in muscle and liver, which entails a decrease in fatty acid oxidation and an increase in body fat. As it turned out, almost all known cardiovascular risk factors are to a greater or lesser extent interconnected with the state of the intestinal microbiota, so understanding its role and methods for correcting the composition of the intestinal microbiota can be of great importance in solving important issues in medicine