CONTENT OF MINERAL ELEMENTS IN HYPATOCYTES OF RATS WHO HAVE INSULIN RESISTANCE, OBESITY AND OBESITY IN COMBINATION WITH IODIDEFICIATE

The article covers the topic of mineral elements in hepatocytes of rats with insulin resistance, obesity and obesity in combination with iodine deficiency. According to modern concepts, Ir and obesity are the root pathophysiological processes that lead to the cascade of pathological reactions. The result of that reactions is the formation of a whole set of disorders and diseases. That's why it is crucial to study fundamental mechanisms of the development of that disorders. Studying of the pathogenesis of Ir and obesity in the terms of the state of macro- and micronutrient provision, understanding of the peculiarities of pathogenetic and therapeutic significance of the level of macro- and microelements - can be the basis for the development of new methods of prevention and treatment of these pathologies. It is known from literary sources that the pathological process in the liver may lead to changes in the metabolism of iron. Considering that the main function of iron is its participation in oxidative-reduction reactions, the result can be explained by the increase of oxidative processes in hepatocytes. It can be assumed that the increase of the level of calcium in hepatocytes leads to the launch of the mitochondrial apoptotic signaling cascade, since this cation plays an important role in the mechanisms of death of liver cells. As it is known from literary sources, the development of insulin resistance is associated, above all, with the deficiency of magnesium. According to clinical and fundamental studies, Magnesium has a hepatoprotective effect. Removal of magnesium from hepatocytes may be associated with a decrease in the content of ATP. It was investigated that magnesium ions act as the essential cofactors of many enzymes involved in the metabolism of carbohydrates and fats, while its low level increases the index of atherogenicity, which is a factor of ali-mentary obesity. Probably, the violation of hepatocyte metabolism leads to the generation of AFK, which causes the release of zinc from proteins, resulting in their dysfunction. The results can be explained by the increased use of zinc in the production of zincall2-glycoprotein, which increases with alimentary obesity, having, according to scientists, a protective role. Mangan activates the enzymes of the citric acid cycle, enhances the action of insulin necessary for its synthesis. Since Mangan is an important bioelement that strengthens the hypoglycemic effect of insulin, counteracts fatty liver degeneration, the tendency to determine its content in animals of all experimental groups can be explained by the development of pathological process in hepatocytes. Violation of metabolism in the liver causes a rapid decrease in the content of Chromium. The achieved results demonstrate changes in the content of mineral elements in animal groups with insulin resistance, obesity and obesity in combination with iodine deficiency. Further research of the features of metabolism of bioelements in the liver tissue will lead to the better understanding of the biochemical mechanisms of the development of these pathologies. Furthermore, it will create opportunities for a comprehensive correction of other metabolic changes.