Епідеміологія метаболічного синдрому та концепції механізмів його розвитку

Abstract

The purpose of the study was to analyze literary sources with the study of modern views on the epidemiology of the metabolic syndrome and pro-inflammatory concepts of the mechanisms of the development of insulin resistance and type 2 diabetes mellitus, as one of its components. Materials and methods. Analytical and bibliosemantic methods were used in the research. During the scientific search, 53 sources of modern domestic and foreign literature were reviewed and analyzed. Results and discussion. Metabolic syndrome is the most common disorder of endocrine regulation, which is one of the threatening health care problems of the 21st century. In recent years, it remains almost the most important problem of endocrinology, cardiology, dietology, internal and family medicine. In recent decades, foreign researchers assign the most important role in the mechanism of metabolic syndrome development to adipocytes of adipose tissue. Most scientists consider insulin resistance to be the pathogenetic basis of metabolic syndrome. Insulin resistance manifests itself as the resistance of body cells to the action of insulin and occurs as a result of a violation of the insulin signal in these cells, the implementation of which is carried out by a membrane-mediated mechanism. Molecular manifestations of insulin resistance should be sought among the components of the insulin cascade, which includes the receptor, the substrate of the insulin receptor (IRS protein), the PI3-kinase cascade, and the GLUT-4 glucose transporter activation system. It should be noted that within the framework of the relationship between obesity, inflammation and insulin resistance, the following cytokines, TNF-α and IL-6, deserve more attention. TNF-α reduces the tyrosine protein kinase activity of the insulin receptor, the insulin-stimulated phosphorylation of its substrates (serine phosphorylation) and the expression of matrix ribonucleic acid GLUT-4 in muscle and adipose tissues, which is accompanied by impaired glucose transport. Also, TNF-α reduces the expression of the lipoprotein lipase gene, stimulates lipogenesis and synthesis of fatty acids, which additionally increases the degree of IP and obesity. IL-6 reduces the expression of the transporter GLUT-4 and the substrate of the insulin receptor, while also having an anti-inflammatory effect due to the reduction of TNF-α and interferon. Under the influence of this cytokine, the level of glycerol and free fatty acids in blood serum increases, which is accompanied by a lipotoxic effect on β-cells of the pancreas. Conclusion. Metabolic syndrome is a pathological process, the spread of which has become epidemic both in developed foreign countries and in Ukraine. One of the important components of the pathogenesis of the metabolic syndrome is insulin resistance, the mechanisms of which, in particular, are related to pro-inflammatory cytokine-mediated mechanisms affecting insulin signaling, glucose transport, involved in pathological changes in lipid synthesis and metabolism, as well as pro-oxidant and cytotoxic processes