Peculiarities of the Relationship Between Microbiome, Matrix Metalloproteinases and Morphological Changes of Epithelium in Patients With Functional and Organic Intestinal Pathology

Abstract

Hypercaloric nutrition of rats negatively affects the functional state of the endocrine part of the pancreas and leads to an imbalance in blood plasma parameters. Malnutrition leads to hyperinsulinemia, while glycemia levels remain elevated, requiring the production of even more insulin by pancreatic β-cells. Gradually, chronic compensatory hyperinsulinemia develops, which is secondary and has an adaptive value for reducing glycemia. The absence of adequate glucose levels for insulin release leads to a shift in the balance between hormones towards counterinsulin factors that stimulate lipolysis, glycolysis, and gluconeogenesis, with the subsequent development of hyperglycemia. High levels of unesterified fatty acids inhibit glycolysis. Ultimately, the metabolism of fatty acids produces ketone bodies, which reflect intracellular glucose deficiency and, under conditions of oxygen deficiency, can damage cell membranes and disconnect oxidation and phosphorylation in the mitochondria of cells. High levels of unesterified fatty acids and glucose have a joint inhibitory effect on the use of each other as an energy source: when unesterified fatty acids are available as energy substrates, their metabolism causes high levels of acetyl-CoA in mitochondrial cells, which leads to impaired use of glucose as an energy source. The established hormonal-substrate relationships due to the consumption of excessive amounts of fats and carbohydrates in the diet of rats reflect pancreatic hyperfunction and associated metabolic disorders, which is a risk factor for the development of functional pancreatic disorders in animals.