METABOLIC SYNDROME IN THE PHYSICIAN POPULATION

Аннотация

Metabolic syndrome (MS) is a cluster of conditions, including abdominal obesity, insulin resistance, type 2 diabetes mellitus, arterial hypertension, and dyslipidemia, which significantly increase the risk of cardiovascular diseases. This study examines MS among physicians, analyzing its genetic predisposition, external risk factors, and pathophysiological mechanisms. The role of insulin resistance, adipocyte dysfunction, and free fatty acids in exacerbating metabolic disturbances is discussed. Various definitions and diagnostic criteria for MS are compared, highlighting inconsistencies in global prevalence estimation. Finally, pharmacological interventions, particularly metformin, are reviewed as a treatment option forMS when lifestyle modifications prove insufficient. Kеywоrds: Metabolic Syndrome, Insulin Resistance, Type 2 Diabetes Mellitus, Obesity, Cardiovascular Disease, Dyslipidemia. INTRОDUСTIОN More than 20 years have passed since the first description of metabolic syndrome (MS) in adults [1]. According to the majority of scientists actively involved in the study of this pathology, the main components of MS are: abdominal obesity, impaired glucose tolerance (diabetes mellitus - type 2 DM), arterial hypertension, dyslipidemia [2]. Based on numerous studies, it has been noted that the presence of MS increases the risk of early development of cardiovascular diseases not only in adults, but also in children [3]. In this regard, early identification of risk groups of children for the development of obesity and MS is necessary, sincepreventivemeasures can reduce mortality from cardiovascular pathology [4]. MАTЕRIАLSАND MЕTHОDS In addition to a predisposition to the main components of MS, a familial predisposition to the development of non-alcoholic fatty liver disease (NAFLD) has been noted. A study involving parents and children found that in families where 37% of parents suffered from NAFLD, fatty liver dystrophy was present in 17% of brothers and sisters, and in families in which NAFLD was detected in 78% of parents, 59% of brothers and sisters suffered from this pathology [1]. An interesting fact is that early development of obesity in the father increases therisk ofNAFLD in children [2]. RЕSULTSАNDDISСUSSIОN The pathogenesis of disorders in MS is based on insulin resistance (IR) [1] (see figure). Genetic factors play a significant role in the development of IR, which are expressed in constitutional features of the composition of muscle fibers, fat distribution, activity and insulin sensitivity of key enzymes of carbohydrate and fat metabolism [3]. In addition to genetic factors, there are many external and internal causes that lead to a decrease in tissue sensitivitytoinsulin and the risk of developing MS:infections, injuries, stress, alcohol abuse, 98,7:ROTCAFTCAPMI.SECNEICS LACIDEM,5202, yraurbeF,5emuloV gro.srehsilbupcimedaca.www increased activity of the sympathetic nervous system, the level of counter-insular hormones and other neurohormonal disorders [4]. A special role of abdominal obesity in the development of IR has been noted [2]. As a result of the fact that the adipocytes of visceral adipose tissue have reduced sensitivity to the antilipolytic action of insulin and increased sensitivity to the lipolytic action of adrenergic stimuli, excessive breakdown of triglycerides occurs in visceral fat cells with the formation of free fatty acids (FFA) [1]. In addition, adipocytes with excess lipid deposition become even more insensitive to the action of insulin and serve as a site of intensive breakdown of triglycerides. Most of the FFA from visceral adipose tissue enters directly into the portal vein through a wide network of capillaries communicating with the vascular system of the liver. When entering hepatocytes, FFAs in significant quantities exert their adverse effects, leading to structural changes in the phospholipids of cell membranes, disruption of the expression of genes that control the conduction of the insulin signal into the cell, thereby reducing the number of insulin receptors and the binding of insulin to hepatocyte receptors, aggravating IR at the liver level [2]. Another portion of FFAs enters the systemic circulation and leads to excessive accumulation of FFAs in the intercellular spaces of skeletal muscles, preventing the utilization of glucose by myocytes and contributing to a decrease in peripheral sensitivity to insulin[3]. It has been shown that lipid deposition in the intercellular spaces of skeletal muscles is present already at the initial stages of obesity development in children [4]. With insufficient sensitivity of cells to insulin, glucose transport into cells is disrupted and hyperglycemia occurs. In order to maintain normal glucose concentration in the blood, the pancreas is forced to synthesize more insulin, resulting in hyperinsulinemia, which subsequently contributes to its decompensation [2]. The situation is aggravated by free fatty acids, which have a “lipo