Abstract

This literature review is devoted to the relationship of the structural features of the metabolic syndrome in proliferative processes and endometrial cancer (EC), and the identification of the relationship between the individual components of the metabolic syndrome and the development of endometrial cancer. The metabolic syndrome is currently a global medical and social problem, which is due to the wide spread of this symptom complex in the population. Today, the main concept of this syndrome is the concept of a cluster of components associated with an increased risk of developing type 2 diabetes and cardiovascular diseases. It is known that an increase in the mass of adipose tissue above the norm by 20% or more leads to dysfunction of the hypothalamic-pituitary-ovarian system. At the same time, the risk of RE on the background of metabolic syndrome increases by 2-3 times. This probability also largely depends on the severity of proliferation in the endometrium, which is caused by the presence of dyshormonal and metabolic disorders. In addition, this is due to the aggravation of insulin resistance, an increase in the production of androgens by the ovaries, the formation of stable anovulation and, as a result, the progression of pathological changes in the endometrium. With the onset of peri - and postmenopausal endometrial hyperplasia in about 50% of cases progressing to malignant pathology. The role of the system of insulin-like growth factors, adipokines secreted from visceral adipocytes of free fatty acids, local estrogen formation and hyperandrogenization is also recognized in creating a predisposition to the EC formation. According to the results of the study of the functioning of the autocrine-paracrine system of adipose tissue, the risk of endometrial proliferative processes is higher at low levels of adiponectin and high levels of insulin. All this indicates the feasibility of monitoring the status of adipose tissue.

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