Muscle capillarization, their morphology and pathogenesis of metabolic syndrome

Abstract

Morphological changes in muscles associated with a decrease in the number of fast, oxidizing muscle fibers of type IIA and an increase in the number of fast, glycolytic muscle fibers of type IIB, as well as a violation of the blood supply to muscle tissue, were considered by us in many pathological conditions associated with insulin resistance. Violation of tissue blood supply, closely associated with a decrease in sensitivity to insulin and the degree of hypertension, occurs at a relatively early stage, while an increase in the number of muscle fibers of type IIB occurs later and is associated with an increase in the concentration of atherogenic factors and hyperlipidemia. Type IIB muscle fibers (MF) are the most insulin-insensitive type MF and are not adapted to fat oxidation during muscle work. This contributes to the further development of insulin resistance and obesity; while the excess of fatty acids is sent to the liver, again violating its function. Excessive insulin also inhibits the liver. Hyperinsulinemia leads to inhibition of the synthesis of specific proteins such as the protein transporting testosterone (a sex hormone-binding globulin). As a result, an increased concentration of free testosterone leads to virilization of women and the further development of insulin insensitivity. In contrast to the previously existing concept, which assigned the main role to intra-abdominal adipose tissue, muscles and liver should also be considered as organs involved in the pathogenesis and development of the metabolic syndrome.