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METABOLIC SYNDROME IN THE PHYSICIAN POPULATION
Umarova Z.
Andijan State Medical Institute
Abstract:
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
for MS 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,
since preventive measures can reduce mortality from cardiovascular pathology [4].
MАTЕRIАLS АND 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 the risk of NAFLD in children [2].
RЕSULTS АND DISСUSSIОN
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
sensitivity to insulin and the risk of developing MS: infections, injuries, stress, alcohol abuse,
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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 “lipotoxic” effect on the -cells of the pancreas, causing a decrease in the sensitivity of
their receptors to the glucose stimulus, which contributes to an increase in the process of
apoptosis of the cells of the islets of Langerhans [2]. Obesity is a chronic disease that is not
always primary, i.e. caused by exogenous factors, in particular, poor nutrition [1]. In
families where parents are obese, lifestyle factors actively contribute to excessive weight
gain in children, who adopt the dietary pattern and level of physical activity of their loved
ones [4]. Secondary obesity has a multifactorial genesis and can be a manifestation of
syndromal genetic pathology, dysfunction of the endocrine or central nervous system, and
also develop as a result of taking medications (for example, glucocorticosteroids) [2]. The
US National Cholesterol Education Program (NCEP) proposed its own criteria for MS,
including central obesity in their list [3]. According to the WHO definition, the fundamental
pathogenetic mechanism of MS development is IR, and according to the NCEP definition,
abdominal obesity is considered the main triggering factor in the development of all
pathological processes within this pathology. In 2003, the American Association of Clinical
Endocrinologists proposed renaming MS to IR syndrome [4]. The presence of multiple
definitions has created the problem of identifying the actual prevalence of MS in different
parts of the world.
СОNСLUSIОN
Drug treatment of MS is carried out only in cases where a set of measures aimed at changing
lifestyle does not lead to sufficiently effective results [3]. Pharmacotherapeutic drugs are
used strictly according to indications, in the absence of contraindications. The choice of
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drugs is carried out in accordance with knowledge of the pathogenesis of the disease. A drug
from the biguanide group, metformin, which is able to increase the sensitivity of div
tissues to insulin, has a proven effect in the fight against IR. Metformin is recognized as the
safest and most effective drug in the treatment of MS and type 2 diabetes in children,
starting from the age of 10, and in adults. Metformin improves cell sensitivity to insulin
through an effect at the genetic level. The most common method is a gradual increase in the
dose of the drug. Metformin is prescribed during meals for an initial course of 6 months
according to the following scheme: 500 mg 1 time during dinner during the 1st week; then
500 mg 2 times during breakfast and dinner in the 2nd week; then 500 mg during breakfast
and 1000 mg with dinner from the 3rd week.
RЕFЕRЕNСЕS
1. Reaven GM. Banting lecture 2018. Role of insulin resistance in human disease. Diabetes
2018; 37: 1535–607.
2. Zakharova IN, Zvenigorodskaya LA, Malyavskaya SI et al. What a pediatrician needs to
know about metabolic syndrome. Part 1. Cons. Med. Pediatrics (Suppl.). 2013; 3: 25–31.
3. Morrison JA, Friedman LA, Gray-McGuire C. Metabolic syndrome in childhood predicts
adult cardiovascular disease 25 years later: the Princeton Lipid Research Clinics Follow-up
Study. Pediatrics 2017; 120: 340–5.
4. Wilson PW, D’Agostino RB, Parise H et al. Metabolic syndrome as a precursor of
cardiovascular disease and type 2 diabetes mellitus. Circulation 2015; 112:3066–72.
5. Miccoli R, Bianchi C, Odoguardi L et al. Prevalence of the metabolic syndrome among
Italian adults according to ATP III definition. Nutr Metab Cardiovasc Dis 2015; 15:250–4.
