Obesity is a serious disease in which fat deposits accumulate in the subcutaneous layer or in the internal organs. There are different types of pathology. One of them is visceral obesity. What it is?

Visceral obesity is a pathology in which fat cells are deposited in internal organs. In most cases, the heart and liver are affected. At the same time, the disease cannot always be noticed externally, because it does not necessarily have to be combined with general obesity.

When an internal organ is damaged, its functioning is disrupted.

The more fat is deposited, the harder it is for the body to work. Over time, adipose tissue affects more and more areas, enveloping the organ from all sides.

As a result, a person faces health problems. Many of them are quite serious and, if ignored, can lead to the death of the patient. Therefore, the disease must be treated when the first signs appear.

It is worth noting that visceral obesity affects not only overweight people, but also thin people. Therefore, it is impossible to judge him by a person’s appearance. To diagnose the disease, an examination of the body is required.

Causes

Visceral obesity develops as a result of exposure to adverse factors or diseases on the body.

The following phenomena can provoke the occurrence of pathology:

1. genetic predisposition.
2. Hormonal imbalance, which often happens in women, especially during the period of bearing and feeding a baby, as well as during menopause.
3. Pathologies of the nervous system, in which a person constantly faces stress, psychosis, and depression.
4. Bad habits. Visceral obesity in men is often associated with the fact that they drink too much beer. When it is consumed, a hormonal imbalance occurs in the body, in which male hormones are replaced by female ones and the process of breaking down fat cells stops.
5. Inactive lifestyle. With sedentary work and lack of physical activity, fat is deposited better.
6. Impaired functioning of the hypothalamus.
7. Wrong nutrition. Obesity occurs among people who consume large amounts of junk food enriched with fats and carbohydrates. To maintain normal body weight, you need more protein than fat.
8. Non-compliance with diet, overeating.
9. Taking certain medications. Most often, rapid weight gain is caused by hormonal drugs, antidepressants, and tranquilizers.
10. Failure of the endocrine system.

If the disease is associated with an unhealthy lifestyle, then curing it is much easier. To do this, you will first need to eliminate factors that influence fat deposition, for example, start following a diet, exercise, and give up bad habits.

Symptoms

In the initial stages, visceral obesity cannot be noticed, since it will be hidden inside. Only over time will the belly begin to enlarge, which will become a cause for concern. The more deposits accumulate, the more symptoms appear.

The following signs of pathology are possible:

1. High blood pressure.
2. Shortness of breath even with slight physical activity.
3. Edema of the lower extremities.
4. Failure in the functioning of the reproductive system, which manifests itself in the form of decreased sexual desire, deterioration of potency, and problems with conception.
5. Rapid heartbeat.
6. Nausea.
7. General weakness.
8. Fast fatiguability.
9. Irritability, depression.
10. Constant desire to eat.

To promptly identify problems with excess weight, you need to regularly use scales. If your body weight is abnormal, you should immediately visit a doctor. There is no need to delay the visit; excess weight should be eliminated in a timely manner.

Treatment Methods

Various methods are used to treat visceral obesity. Successful therapy requires the use of several methods at once.

Nutrition adjustments

The main method of combating obesity is diet. The patient's diet should be balanced and varied. The main part should be proteins, the amount of carbohydrates and fats must be reduced to a minimum. The menu should not contain harmful products.

The following foods are not allowed:

1. Fast food.
2. Smoked meats.
3. Semi-finished products.
4. Sausages.
5. Fat meat.
6. Fatty fish.
7. Sweets.
8. High fat dairy products.
9. Bakery.
10. Confectionery.

The diet includes products such as:

1. Vegetables.
2. Fruits.
3. Berries.
4. Greenery.
5. Lean meats and fish.
6. Fat-free dairy products.
7. Dried fruits.
8. Cereals.

Medicines

Visceral obesity in women and men is not always eliminated by sports and diet; it is often necessary to resort to medications. During therapy, different groups of drugs are used.

In most cases, the drug Orlistat is prescribed. Thanks to it, the patient’s nutritional needs are met, which allows him to eat less.

If the patient also suffers from diabetes, then Metformin is prescribed. With its help, the level of absorption of fatty elements in the intestines is reduced. Analogues of glucagon-like peptide are used to suppress the feeling of hunger.

Under no circumstances should you take various dietary supplements or medications promoted by advertising and other sources. Products are often produced that supposedly help cope with obesity in a short time. Such medications do not bring the desired effect, but only cause harm to health.

Surgical intervention

If treatment of visceral obesity with medications, sports and diet does not help, surgery comes to the rescue. There are several types of operations that can help eliminate pathology.

These include the following:

1. Reducing the volume of the stomach by removing part of it or installing a special ring.
2. Shunt surgery on the small intestine.
3. Liposuction, in which excess fat is pumped out.

After surgical treatment, a rehabilitation period is required. During this time, the patient must refrain from exercise, take vitamins and other medications prescribed by the attending doctor.

Physical activity

Physical activity is one of the main methods of combating excess weight. To get rid of obesity, regular exercise is required. It is advisable to devote time to them daily. You can burn fat in different ways.

But it’s better to combine several activities, for example, doing exercises at home and going to the pool. Gymnastics, swimming, running, race walking and many other methods can help in the treatment of obesity. Your doctor will tell you what is more effective to do.

Why is it dangerous?

Obesity is dangerous to human health and even life. This applies to all types of pathology, including visceral. This is especially dangerous if fatty deposits cover the heart. When there are many of them, they begin to put pressure on the organ and blood vessels.

As a result, blood pressure is disturbed, the patient experiences severe headaches, and the likelihood of developing a heart attack and coronary heart disease increases.

Blood circulation in the body slows down, as a result of which the tissues do not receive enough oxygen and nutrients.

In addition to these problems, the following complications are possible:

1. Metabolic syndrome.
2. Diabetes.
3. Vascular atherosclerosis.
4. Stroke.
5. Menstrual cycle disorders in women.
6. Alzheimer's disease.
7. Formation of malignant tumors.
8. Phlebeurysm.

These pathological conditions are very dangerous to human life. Therefore, it is important to carry out treatment in the early stages of visceral obesity.

Localization of pathology

With visceral obesity, some features of the distribution of fat deposits are observed. However, they differ slightly in male and female patients, which is due to differences in the anatomical structure of their bodies.

Among women

In female patients, fat is most often deposited in places such as:

• hips;
• stomach;
• breast;
• pelvic organs.

In women, fat deposits are distributed more slowly than in men. But the first clinical signs are more vivid.

In men

Men accumulate fat much faster. Doctors explain this by the fact that patients of this sex have large muscle tissues that have some distance between the fibers, into which fat cells become clogged. The most favorite places for obesity in men are the following:

1. Stomach.
2. Shoulders and forearms.
3. Liver.
4. Pancreas.

Thus, visceral obesity is a serious disease that can lead to negative consequences for human health and life. If there are deviations in body weight, you must immediately take measures to eliminate them, preventing the development of the pathology in question.

Exogenous-constitutional obesity is divided into two types - gynoid (gluteofemoral) and android (fat in the abdomen and upper torso). More often, endocrinologists make a second diagnosis. This disease is also called abdominal (“abdomen” in Latin - “stomach”) - the figure begins to resemble an apple due to a bloated abdomen. Fat accumulates in the abdominal cavity, under the skin. If it is localized around the internal organs, such obesity is called visceral (“viscera” - “insides”).

How serious is this pathology and is it possible to achieve a complete recovery after a course of treatment? Let's figure it out.

Essence

So, visceral obesity is excess body weight with fat deposits in the internal organs (the heart and liver primarily suffer). Moreover, external signs of excess weight may not be observed at all.

Whatever organ is attacked by fat, it is no longer able to function at full strength and in the same way. Meanwhile, the adipose tissue grows (in the absence of therapeutic measures), compressing it into a ring. At first, this leads to numerous health complications, and if you don’t catch it in time and lead to third-degree obesity, everything can end in death.

Causes

What causes of visceral obesity are currently known to medicine? Factors that provoke the development of the disease include:

• genetic, hereditary predisposition;
• hormonal disorders during pregnancy, lactation, menopause - in women;
• diseases of the nervous system: constant stressful situations, psychosis, panic attacks;
• beer abuse - in men (testosterone is replaced by female hormones and is no longer involved in the breakdown of fats);
• sedentary lifestyle: lack of active rest, physical exercise, walking;
• improper functioning of the hypothalamus;
• nutritional imbalance, when there are more carbohydrates and fats in the diet than proteins;
• binge eating;
• side effect after taking certain medications: hormones, antidepressants, tranquilizers;
• problems with the endocrine system: hypothyroidism, Itsenko-Cushing syndrome;
• decrease in serotonin (the hormone of happiness, which is also responsible for the feeling of fullness).

If obesity is caused by poor nutrition and a sedentary lifestyle (it is classified as the nutritional type), the chances of recovery are quite high. Here balanced and physical activity comes to the fore.

Everything is much more complicated with genetics and congenital diseases. If the development of pathology is dictated by them, it will be chronic.

Symptoms

Visceral obesity can hide inside the body for a long time. You can suspect it only by weight gain, while the stomach and waist do not grow at first. Therefore, first of all, you need to monitor those extra pounds and not allow them to “exceed” the norm. To do this, BMI is calculated using a special formula: I (BMI) = M (weight in kilograms) / H 2 (height in meters). If the value exceeds 30, immediate action must be taken.

But this is not the only symptom of this disease. Other signs may indicate it:

• hypertension;
• diabetes mellitus type II;
• dyspnea;
• swelling;
• sexual dysfunction, decreased libido, potency, frigidity;
• heart problems: tachycardia, ischemia, bradycardia, etc.;
• liver problems: tingling in the right corner, nausea;
• lethargy, weakness;
• fast fatiguability;
• frequent stress and depression;
• uncontrollable appetite.

To confirm or dispel doubts about the presence of visceral obesity, you can weigh yourself on a special fat analyzer scale before going to the clinic. They are sold in pharmacies and are available in almost every fitness club. For this purpose, doctors will suggest undergoing a computed tomography scan.

Classification

Like any other obesity, visceral obesity can be of 3 degrees. In 1997, WHO presented the following table for ease of classification:

According to the nature of its course, obesity can be stable (weight does not change for a long time), progressive (excess body weight constantly increases), residual (preservation of residual effects after losing weight).

By location:

• - damage to the heart sac by adipose tissue, which disrupts cardiac activity;
• liver (another name for the disease is fatty hepatosis) - dangerous due to intoxication, as bile formation and detoxification are impaired;
• kidneys - disrupts urinary function, causing stagnation of urine, the formation of stones, the development of infectious and inflammatory processes;
• - causes disruptions in the digestive system.

It is possible to clarify the diagnosis, which organ was attacked, only in laboratory conditions - with the help of MRI and ultrasound.

Treatment Methods

It is very important to begin treatment for visceral obesity in a timely manner, before the organ clogged with fat fails to function at all. To do this, you need to make an appointment with an endocrinologist.

The therapeutic course of this disease can be divided into 2 stages:

1. Weight loss (period duration - from 3 months to six months).
2. Its stabilization (from 6 months to 1 year).

Only the joint work of the doctor and the patient can give a chance for recovery. Treatment should be comprehensive, and its main components are diet, sports, behavioral therapy, and in advanced cases, medication and surgery.

Nutrition

Based on the degree of visceral obesity and the patient’s eating habits, the doctor selects the optimal diet.

• reduction in daily caloric intake by 30% than before;
• reducing fats and carbohydrates in the diet;
• all dietary changes are introduced very carefully, gradually;
• are welcome, but without fanaticism: once a week will be enough;
• when creating a menu, you must use lists of permitted and prohibited foods for proper nutrition;
• usually patients with this diagnosis are prescribed dietary table No. 8 according to Pevzner;
• meals should be small but frequent;
• reduce salt to a minimum, replace sugar with honey, avoid fast food and trans fats (especially mayonnaise and ketchup) completely.

When following a diet, you need to remember that the diet must be balanced. Therefore, you cannot give up fats completely, which can lead to disruption of lipolysis, and all therapy will be useless. Therefore, it is better to be under constant supervision of a specialist during this period. He can adjust the menu at any time and give useful advice.

Behavioral Therapy

Physical activity is the main enemy of visceral obesity. But this point of treatment is even more difficult for many patients than the previous one. After all, there you can use your iron character and willpower to do without your favorite hamburger. And then there are the physical activities that obese people perform with great difficulty. Fat folds will put even more pressure on the organs during training, causing fatigue within the first 5 minutes of exercise. Bending over, stretching - everything will be accompanied by profuse sweating, shortness of breath and tachycardia.

Therefore, the regime of aerobic physical activity (frequency of exercises, their type, intensity of training) is selected individually.

Along with exercise, you will need to change your lifestyle, which in many ways has also become the culprit of visceral obesity.

• breathe more fresh air;
• give up alcohol and smoking;
• protect yourself from stress and anxiety;
• sleep at least 8 hours;
• Constantly motivate yourself to move on and not stop there.

In fact, behavioral therapy is rarely described in detail. Nevertheless, it is of great importance for the patient’s recovery.

Drugs

If, 2 months after the start of therapy for visceral obesity using the above methods, the effect is not noticeable, the patient will be offered drug treatment with the following drugs:

1. Orlistat. The course of treatment is from 3 months to 4 years.
2. (Glucophage) reduces the amount of absorbed fat in the intestines and is usually prescribed to patients with concomitant type II diabetes mellitus. Side effects include intestinal disorders.
3. Analogs of glucagon-like peptide give a feeling of false satiety.

Please note that for visceral obesity, the use of herbal, diuretic drugs and all kinds of dietary supplements is not recommended. It must be treated only with “what the doctor ordered.”

The drugs Orlistat and Metformin used in the treatment of visceral obesity

The effectiveness of treatment is assessed within 1 year. During this period, a food diary is kept, the patient’s psychological state is adjusted and constantly monitored.

If the weight does not decrease by more than 10% of the initial weight, the doctor will have to reconsider the treatment tactics: choose a different diet, change the nature of training, replace one pill with another. And continue constant monitoring.

If the target body weight level is nevertheless achieved, a re-examination of risk factors for weight gain and the development of concomitant diseases is carried out.

Surgery

If drug treatment for visceral obesity is ineffective, the patient is offered surgical intervention.

It can be:

• installation of cylinders inside the stomachs, which take away part of the food;
• small intestinal bypass;
• restrictive operations, when the volume of the gastric reservoir is specifically reduced;
• combined surgery (combination of biliopancreatic and gastric bypass).

After such interventions, you will have to go through all the difficulties of the rehabilitation period. Replacement therapy with iron, calcium, and multivitamins is prescribed. It is advisable to sign up for medical and cosmetic surgeries (abdominoplasty and liposuction) only after stabilizing your weight.

Complications

And finally, how dangerous is this disease if it is not treated in a timely manner. It is necessary to immediately take into account the effect of visceral obesity on blood pressure. Fatty tissue envelops the heart and puts pressure on the blood vessels. This results in severe headaches, extreme hypertension, and a high risk of ischemia and heart attack. This slows down blood flow and lymph flow, which leads to oxygen deficiency in all tissues of the body. Moreover, it is not only hypertensive patients who suffer from this.

This pathology can provoke the development of such serious complications as:

• metabolic syndrome (insulin resistance), when the body becomes tolerant to glucose;
• diabetes;
• the formation of cholesterol plaques and the development of atherosclerotic changes;
• stroke and myocardial infarction;
• in women - hirsutism, menstrual irregularities;
• Alzheimer's disease;
• oncology;
• fatty hepatosis;
• varicose veins

These diseases are very serious and life-threatening. Visceral obesity is one of the most insidious. It can hide inside the body for a long time, disrupting the functioning of organs there. It is difficult to treat, but, nevertheless, there is a chance of recovery if the doctor and patient work in close tandem.

OBESITY AND METABOLISM 1 "2004

literature review

Visceral obesity is a key element of metabolic syndrome

S.A. Butrova, F.Kh. Dzgoeva

State Institution Endocrinological Research Center (Dir. - Academician of the Russian Academy of Sciences and Russian Academy of Medical Sciences I.I. Dedov) RAMS, Moscow

The problem of obesity in combination with various metabolic disorders and/or diseases is the focus of modern medical science and healthcare. The prevalence of obesity in the world is so high that it has become a global epidemic. With the spread of obesity across the planet, severe somatic diseases associated with it are multiplying and worsening: type 2 diabetes mellitus (T2DM), arterial hypertension (AH), coronary heart disease, cancer, etc., reducing the quality of life and increasing the mortality rate among the working population. According to WHO experts, 320 thousand people die annually from obesity-related diseases in Europe alone. The most significant medical consequences of obesity are type 2 diabetes and cardiovascular disease (CVD), and the risk of their development is largely determined by the characteristics of adipose tissue deposition in the body.

For the first time, J. Vague drew attention to the problem of the connection between the risk of diseases associated with obesity and the nature of the localization of adipose tissue in his works back in 1947. He identified two types of obesity based on the topography of adipose tissue - android and gynoid - and showed that patients with the android type of obesity more often develop T2DM, hypertension and CVD. Subsequent studies, based on generally accepted criteria for assessing the type of distribution of adipose tissue and indicators of the risk of developing concomitant diseases, proved that abdominal obesity is an independent risk factor for dyslipidemia, disorders of carbohydrate metabolism and the blood coagulation system, independent of the degree of obesity in general. Thus, data from the Gothenburg study confirmed that the waist-to-hip ratio (WC/HR) is an independent risk factor for myocardial infarction, stroke, and mortality from them; OH&S has a closer connection with these

diseases than body mass index (BMI).

With the introduction of computed tomography (CT) and magnetic resonance imaging (MRI) into medical practice, the abdominal type of obesity was divided into two subtypes - abdominal-visceral and abdominal-subcutaneous. It turned out that it is abdominal-visceral obesity that is usually combined with an unfavorable metabolic profile. In the works of J.-P. Despres, B. Wajchenberg and many other researchers have shown that the area of ​​visceral fat in men is more than 130 cm2, and in pre- and postmenopausal women more than 110 cm2 indicates an increased risk of coronary heart disease. A clear correlation was found between the area of ​​visceral adipose tissue, determined by CT and MRI, and the WC indicator.

The dangerous threshold for the accumulation of visceral adipose tissue - 130 cm2 in people of both sexes under 40 years old - corresponds to a waist circumference of more than 100 cm, and at the age of 4060 years - already from 90 cm. Research by T. Han et al. , like other works based on a comparison of the total health risk with waist circumference indicators for abdominal-visceral obesity, confirmed by computed tomography, revealed that with a WC of 94-101 cm in men and 8087 cm in women, there is an increased risk, and with an even Higher WC values ​​indicate a high risk of developing CVD and T2DM. Y Matsuzava et al., using CT to determine the topography of adipose tissue in the abdominal region, showed that the accumulation of fat in visceral depots, even with normal BMI values, is usually accompanied by metabolic and hemodynamic disorders, and in 40% of patients with coronary disease heart there is visceral obesity with normal body weight.

In recent decades, various hormonal and metabolic disorders and/or diseases associated with obesity have been considered in

complex, since almost each of them, being a risk factor for the development of CVD, in combination greatly increases the risk of developing macrovascular atherosclerotic diseases. In 1988, G. Reaven described the so-called “syndrome X”, combining arterial hypertension, dyslipidemia and carbohydrate metabolism disorders, and for the first time suggested that the unifying basis of these disorders could be insulin resistance (IR) and compensatory hyperinsulinemia (HI). In 1989, N. Kaplan described the “deadly quartet”, including abdominal obesity among the most important components of the syndrome along with hypertension, impaired glucose tolerance and hypertriglyceridemia. In the 90s, metabolic disorders and diseases developing in obese individuals were united under the umbrella of “metabolic syndrome.”

The meaning of introducing this concept into scientific terminology is that it combines a complex of hormonal and metabolic disorders and diseases that significantly accelerate the development and progression of atherosclerotic vascular diseases, which, according to WHO experts, rank first among the causes of mortality in the industrialized countries of the world. Many modern researchers consider metabolic syndrome as a prelude to diabetes mellitus.

With the development of the concept of metabolic syndrome, its scope has expanded, combining the following symptoms and manifestations:

Abdominal-visceral obesity,

Insulin resistance and hyperinsulinemia,

Dyslipidemia,

Arterial hypertension,

Impaired glucose tolerance/diabetes mellitus type 2,

Early atherosclerosis/IHD,

Hemostasis disorders

Hyperuricemia and gout,

Microalbuminuria,

Hyperandrogenism.

In recent years, many researchers have proposed including hepatic steatosis and obstructive sleep apnea syndrome as components of the syndrome. The prevalence of metabolic syndrome in the general population is quite high. According to the Health and Nutrition Examination Study (NHANESIII), conducted in the United States from 1988 to 1994 and covering almost 9,000 men and women, metabolic syndrome - according to the Adult Treatment Panel III (ATPIII) criteria - was identified in 6.7% of patients in age 2029 years, 43.5% in the age group 60-69 years and 42% - 70 years and older. The specificity of the US population allowed us to identify ethnic differences in the prevalence of metabolic syndrome in this study: it is more common in patients of Spanish origin (32%) compared to other ethnic groups (20-24%).

In terms of population, NHANES III results showed that metabolic syndrome in the United States affected 24% of the population, which was approximately 47 million people.

The identified ethnic characteristics of predisposition to the development of metabolic syndrome confirm the role of genetic factors. At the same time, the increasing number of patients with this pathology in all regions of the planet can be regarded as the result of the interaction of modern lifestyle and genotypic characteristics.

According to P. Zimmet, published in 2003, about a quarter of the population of Western Europe has impaired glucose tolerance or metabolic syndrome. The latter is most common in northern European countries. According to epidemiological studies conducted in Finland and Sweden, 10% of women and 15% of men have metabolic syndrome without carbohydrate metabolism disorders.

In Russia, according to the results of the WHO MONICA study, 40% of the unorganized population of Novosibirsk aged 25-64 years have 2 or more components of the metabolic syndrome with a predominance of its prevalence among women (the study used the definitions of this pathology developed by WHO).

When studying the incidence of metabolic syndrome among obese patients who applied to the Research Center of the Russian Academy of Medical Sciences, it was identified (according to the diagnostic criteria of the ATRS) in 49%, and in the age group from 16 to 22 years in 35% of patients.

For the first time, diagnostic criteria for metabolic syndrome were developed and formulated by a WHO working group. However, the ATPIII criteria for diagnosing metabolic syndrome, published in 2001 by the National Cholesterol Education Program's expert committee, are more consistent with clinical practice (see table).

In the proposed definitions of metabolic syndrome, an independent place is given to visceral obesity. This is substantiated by the results of a number of large studies that have demonstrated a close relationship between abdominal-visceral obesity and a complex of hormonal and metabolic risk factors that form the basis of this problem.

Diagnostic criteria for metabolic syndrome

Risk factors Meaning

Abdominal obesity Waist circumference

Men > 102 cm

Women > 88 cm

Triglycerides > 3.95 mmol/l

Men< 1,1 ммоль/л

Women< 1,3 ммоль/л

Blood pressure > 130/ > 85 mm Hg. Art.

Fasting blood glucose > 6.1 mmol/l

OBESITY AND METABOLISM 1 "2004

a decrease in the binding of insulin by hepatocytes and its degradation and the development of IR in the liver, inhibition of the suppressive effect of insulin on glucogenesis, as well as systemic hyperinsulinemia, which in turn contributes to the development of peripheral insulin resistance [8,9,30].

An independent effect of FFA on glycogenolysis and gluconeogenesis is also assumed.

Once in the systemic circulation, FFAs contribute to impaired glucose uptake and utilization in muscle tissue through the Randle cycle and, thus, increase peripheral insulin resistance. Excessive FFA content in the blood serves as a source of accumulation of triglycerides and products of non-oxidative metabolism of FFA in skeletal muscles and heart muscles and, accordingly, disruption of insulin-dependent glucose utilization in these tissues. It has also been shown that FFAs have a direct toxic effect on pancreatic beta cells (lipotoxicity effect).

Under conditions of insulin resistance and excess FFA, lipid metabolism is disrupted and atherogenic dyslipidemia develops. Due to a slowdown in the catabolism of triglycerides and triglyceride-rich lipoproteins, increased accumulation of very low density lipoproteins (VLDL), cholesterol esters accumulate in macrophages, and an increase in the level of modified low density lipoproteins (LDL), which have a high ability to oxidize and penetrate into the subendothelial space of the vascular walls, high affinity for proteoglycans and reduced affinity for LDL receptors. All these properties contribute to the active inclusion of small dense LDL particles in the process of atherogenesis.

Along with impaired lipid metabolism under conditions of insulin resistance and hyperinsulinemia, there is an increase in the proliferation of smooth muscle cells, fibroblasts, and collagen synthesis, which also contribute to the development of atherosclerotic vascular damage.

Among the adipokines secreted by adipose tissue and influencing the development of the components of the metabolic syndrome, the most studied currently are leptin, tumor necrosis factor-a and adiponectin.

Leptin is a multifunctional adipose tissue hormone secreted by adipocytes in proportion to the mass of adipose tissue. The effect of leptin on the central nervous system, a number of neuroendocrine functions, the immune system, bone metabolism, lipid and carbohydrate metabolism has been proven (Fig. 1). The leading function of leptin, as recent studies have shown, is the protection of peripheral tissues from ectopic accumulation of lipids. According to H. Unger and L. Orci, leptin is an antisteatogenic hormone and, like insulin, which regulates glucose homeostasis and prevents the development of glucotoxicity, regulates the homeostasis of fatty acids, protecting against the development of lipotoxicosis. The effect of leptin on insulin resistance was

Glucose absorption and metabolism

Leptin

- "Glucose absorption,

Fat deposition and fat metabolism / Homeostasis

glucose tissue

Rice. 1. Effects of leptin.

trivial syndrome. The close connection between abdominal obesity and cardiovascular risk factors allowed ATRS specialists to define metabolic syndrome as a set of metabolic complications of obesity. The key link that unites various disorders that develop in metabolic syndrome is primary insulin resistance and compensatory hyperinsulinemia.

The pathogenesis of IR in visceral obesity is heterogeneous in nature and is determined by the interaction of a number of factors: genetic, gender, age, hormonal influences, conditions of intrauterine development, external influences, etc. The results of recent studies have shown that adipose tissue secretes a number of active molecules - adipokines, which influence on food consumption, metabolic processes, the formation of oxidative stress and disorders of the cardiovascular system, i.e., having various local, peripheral and central effects. Many studies emphasize that in obesity, the development and progression of insulin resistance and its various manifestations may be a reflection of the lipotoxic effects of free fatty acids and adipokine imbalance. Consequently, the adipose tissue itself, providing a large amount of FFA and cytokines into the bloodstream, is a key factor in the development of the main disorders and manifestations of the metabolic syndrome.

According to many researchers, the topographic and metabolic features of visceral adipose tissue are decisive in the development of insulin resistance and complications of obesity (portal theory).

With the predominant deposition of fat in the visceral region, FFAs released due to intense lipolysis enter the portal vein and liver in large quantities. It leads to

identified by studying metabolic parameters in leptin deficiency syndromes, which are accompanied by hyperphagia, obesity, hypercortisolemia and type 2 diabetes. The administration of exogenous leptin contributed to the normalization of metabolic parameters regardless of the dynamics of body weight, which served as the basis for the conclusion about the independent role of leptin in influencing insulinemia and insulin resistance.

A number of authors do not exclude the possible influence of leptin on insulin sensitivity through direct effects at the level of peripheral tissues. In visceral obesity, the combination of increased plasma concentrations of FFA, triglycerides, LDL, chylomicrons and peripheral leptin resistance, developing against the background of hypercortisolemia, leads to the deposition of fatty acids in the form of triglycerides in skeletal muscles, liver, heart muscle, and pancreas. Excessive TG deposition in organs is a potential source of FFA entering cells in quantities significantly exceeding their oxidative needs.

Normally, with an excess supply of fatty acids into tissues, the activity of FFA oxidation enzymes increases, and unused energy is dissipated in the form of heat using acyl-CoA reductase and UCP-2, that is, the system of so-called compensatory FFA oxidation is turned on. It is obviously enhanced by FFAs themselves, which are ligands of PPAR-y, which increases the expression of enzymes at the final stages of this process. This compensatory oxidation system requires normal functioning of the leptin system. With leptin resistance, compensatory oxidation of FFAs does not occur; the non-oxidative pathway of their metabolism (peroxidation and formation of ceramides) is activated. The accumulation of unoxidized metabolites of free fatty acids and ceramides can stimulate the development of lipotoxic disorders, the end result of which is manifestations of metabolic syndrome: insulin resistance, hyperlipidemia, diabetes mellitus, cardiomyopathy, increased blood pressure (BP). When the action of leptin is disrupted, there is also an increase in de novo synthesis of fatty acids from glucose due to overexpression of a number of proteins involved in the process, and this synthesis occurs regardless of the concentration of FFA.

In conditions of visceral obesity and leptin resistance, the effect of leptin on vascular calcification, accumulation of cholesterol by macrophages, initiation of oxidative stress, increased tone of the sympathetic nervous system, and increased blood pressure is likely to increase. All these factors together reduce the compliance of arteries with respect to atherosclerotic processes. Thus, in visceral obesity, disruption of the action of leptin may be one of the leading factors in the development of insulin resistance, dysfunction of β-cells and the processes of atherogenesis.

Adiponectin-

Oxidation

FFA oxidation| 3 Glucose| TG|

Vascular h¡

i inflammation

Insulin sensitivity t

Rice. 2. Proposed effects of adiponectin.

One of the unique products secreted by adipose tissue is adiponectin. However, unlike other adipokines, the secretion of which increases in proportion to the increase in adipose tissue mass, its level in obesity is lower than in people with normal body weight. The experimental data obtained demonstrated the inhibitory effect of adiponectin on the differentiation of pre-adipocytes, which confirms its possible effect on the regulation of body fat mass. TNF-α, interleukin-6 (IL-6) and PPARY are involved in the expression and secretion of adiponectin itself. Multicenter studies have shown that plasma adiponectin levels are inversely associated with obesity, adipose tissue mass, WC/TB, dyslipidemia, cardiovascular disease, and insulin resistance.

A decrease in adiponectinemia has a closer correlation with hyperinsulinemia and insulin resistance than with obesity in general and adipose tissue mass. A prospective study among Pima Indians found that low plasma adiponectin levels preceded the onset of insulin resistance. The experiment showed that adiponectin helps reduce insulin resistance by stimulating tyrosine phosphorylation of the insulin receptor, and also reduces the flow of fatty acids into the liver and stimulates their oxidation by activating protein kinase, helping to reduce the production of glucose by the liver and the synthesis of VLDL triglycerides. In muscle tissue, adiponectin, like leptin, stimulates the oxidation of FFAs, reduces intramyocellular lipid accumulation and improves the sensitivity of muscle tissue to insulin (Fig. 2). It is possible that adiponectin stimulates the oxidation of FFAs through the expression of genes encoding CD36, acyl-CoA oxidase and uCP-2, as well as activation of AMP protein kinase.

OBESITY AND METABOLISM 1 "2004

OBESITY AND METABOLISM 1 "2004

The European Prospective Investigation into Cancer and Nutrition found that low levels of adiponectin were independently correlated with an increased risk of developing T2DM in relatively healthy people. The results of scientific work have given grounds for many researchers to consider adiponectin as a marker of insulin resistance in patients with type 2 diabetes.

Clinical studies have also shown that low levels of adiponectin are associated with an atherogenic lipid profile and high blood pressure. M. Matsubara et al. found that in women without carbohydrate metabolism disorders, the concentration of adiponectin in the blood plasma has a clear negative correlation with the atherogenic index (TC/HDL cholesterol), the level of triglycerides and apolipoproteins B and E, as well as a positive correlation with HDL and apoprotein A-1.

K. Hotta et al. reported a pronounced negative correlation of adiponectin levels with triglycerides and a positive correlation with HDL in patients with type 2 diabetes. It was also shown that in patients with type 2 diabetes and coronary artery disease, adiponectin levels are lower than in patients without coronary artery disease, which may indicate its antiatherogenic properties. properties. Hypoadiponectinemia, present in patients with metabolic syndrome, may contribute to the increase in atherosclerotic changes in them. Administration of recombinant adiponectin to such patients leads to an increase in the suppressive effect of insulin on gluconeogenesis. This effect is associated with a decrease in the expression of gluconeogenesis enzymes such as glucose-6-phosphatase and phosphoenolpyruvate carboxykinase.

The discovered relationship between low levels of adiponectin, obesity, insulin resistance, coronary heart disease and dyslipidemia allows us to consider adiponectin as another marker of metabolic syndrome.

The works of Japanese scientists have shown that adiponectin inhibits the adhesion of platelets to the endothelium, suppresses the transformation of macrophages into foam cells, inhibits the proliferation and migration of myocytes, the capture of LDL by the developing atherosclerotic plaque, suppresses the activity of myelomonocytes, phagocytes and reduces the production of TNF-a by macrophages. Moreover, adiponectin was found to have an inhibitory effect on growth factor-mediated proliferation of smooth muscle cells in the aorta.

Physiological concentrations of adiponectin suppress the expression of adhesion molecules. One of the most important antiatherogenic mechanisms of action of adiponectin - suppression of monocyte adhesion to the endothelium - occurs by reducing the activity of nuclear transcription factor kappa B (NTF-κB), blocking phosphorylation of its subunit I-κB. Moreover, adiponectin was found to have an inhibitory effect on growth factor-mediated proliferation of smooth muscle cells in the aorta. The listed protective

The specific mechanisms of adiponectin in relation to the development of atherosclerosis are lost in obesity, especially in its abdominal-visceral subtype. In addition, visceral adipose tissue secretes a number of cytokines that suppress the action of adiponectin, the main of which is tumor necrosis factor-a.

Many publications have noted a positive correlation between the expression of TNF-a and the values ​​of WC/TB, BMI, systolic blood pressure, as well as a decrease in the expression of TNF-a and its concentration in the blood with a decrease in body weight. The mechanism of action of TNF-a on insulin sensitivity is to reduce the activity of insulin receptor tyrosine kinase and increase the phosphorylation of serine, the substrate of the insulin receptor, as well as to inhibit the expression of GLUT-4 in muscle and adipose tissue. TNF-a also inhibits adipocyte differentiation. It is believed that this cytokine has auto- and paracrine effects and is most important for the development of insulin resistance in adipose tissue. TNF-α may also contribute to the development of insulin resistance by stimulating lipolysis in adipocytes.

In obesity, TNF-a plays an important role in increasing the expression of plasminogen activator inhibitor-1 (PAI-1), the production of leptin, interleukin-6 and reducing the expression and activity of adiponectin. TNF-a stimulates the activation of the nuclear transcription factor kappa B, which increases the production of NO - the basis of the inflammatory response in the vascular wall, intracellular adhesion of monocytes and the entire cascade of oxidative stress. One of the effects of YTP-κB is disruption of the insulin receptor signal and the development of insulin resistance.

It has been shown that in proportion to the increase in the mass of adipose tissue in the blood, the concentration of interleukin-6 increases. The production of interleukin-6 by omental adipose tissue is 2-3 times higher than that by subcutaneous abdominal adipose tissue. Due to the specific location of visceral adipose tissue, IL-6 secreted by it has the ability to directly influence metabolic processes in the liver by suppressing the sensitivity of liver insulin receptors. This adipokine stimulates the formation of C-reactive protein, which is a marker of the inflammatory process of the vascular wall. IL-6 reduces the expression of lipoprotein lipase, having a local effect on the absorption of FFA by adipocytes, increases the production of triglycerides, which may be important for the development of hypertriglyceridemia in visceral obesity. This cytokine also has a direct stimulating effect on the hypothalamic-pituitary-adrenal system and has a positive correlation with insulin resistance, the development of T2DM and myocardial infarction. It has been established that in patients with abdominal obesity, adipose tissue of the omentum is the main source of increased levels in the blood plasma of in-

plasminogen activator inhibitor-1. At normal body weight, PAI-1 synthesis occurs mainly in hepatocytes and endothelial cells, and to a lesser extent in smooth muscle cells and platelets. PAI-1 is a serine protease inhibitor and a major regulator of the fibrinolytic system. It binds and inhibits tissue-type plasminogen activators and urokinase, which modulate endogenous fibrinolysis. As many authors testify, a high level of PAI-1 is an independent predictor of myocardial infarction in men with coronary artery disease. A number of prospective studies have shown a relationship between increased levels of PAI-1 and the risk of developing atherosclerosis and thrombosis, especially coronary thrombosis. In obesity, there is increased expression of the PAI-1 gene and a clear positive correlation between PAI-1 levels and metabolic syndrome parameters, especially between the levels of fasting glucose and insulin, triglycerides, LDL cholesterol, visceral adipose tissue mass and BMI.

In 2001, a polypeptide, resistin, was isolated, which is secreted mainly by preadipocytes and to a lesser extent by mature adipocytes, mainly of abdominal localization. Experiments have shown that administration of recombinant resistin to mice without obesity leads to the development of insulin resistance, and administration of antiserum to resistin improves insulin sensitivity in obese animals with IR. According to experimental data, resistin neutralizes the inhibitory effect of insulin on glucose production by the liver and reduces glucose uptake by skeletal muscles, regardless of GLUT-4. However, the role of resistin in the mechanisms of development of IR is not yet clear enough: there are studies that failed to confirm its role in the pathogenesis of insulin resistance in obesity. In addition, most of the known mechanisms of action of resistin were found in experiments with mice, and human resistin is only 59% similar in structure to mouse resistin.

It has been established that adipose tissue is the second source of angiotensin secretion after the liver, and its expression is more pronounced in visceral than in subcutaneous adipocytes. Enzymes that convert angiotensinogen to angiotensin I and angiotensin II are also expressed in adipose tissue. Angiotensin II, produced by adipose tissue, accelerates the differentiation of preadipocytes into adipocytes by stimulating the production of prostaglandin K. It has also been suggested that increased production of angiotensinogen through angiotensin II may be important in the mechanisms of arterial hypertension in obese patients. Angiotensin II is a proatherogenic protein that stimulates intracellular adhesion of molecules into the vascular wall, the formation of free radicals, and disruption of the integrity of the vascular wall. All these processes provoke endothelial dysfunction.

Almost all components of the metabolic syndrome - abdominal-visceral obesity,

Mechanisms of development of type 2 diabetes mellitus and atherosclerosis in obesity

(after Ch. Lyon, R. Law and W hsueh, 2003)

Insulin resistance

Metabolic syndrome

Diabetes mellitus type 2

Endothelial dysfunction

f Oxidative stress f Inflammatory response f Atherosclerosis

f f f Atherosclerosis

IR and GI, dyslipidemia, hypertension, IGT/DM2, early atherosclerosis/CHD, hemostasis disorders, hyperuricemia and gout, microalbuminuria, hyperandrogenism

They are established risk factors for the development of cardiovascular diseases; their combination greatly accelerates the development of CVD.

Recently, in connection with the in-depth study of the molecular mechanisms of the inflammatory reaction of the vascular wall in the pathogenesis of the formation of atherosclerotic plaque, the influence of the nuclear transcription factor kappa B has attracted increasing interest. An increase in the levels of TNF-a, FFA, IL-6, PAI-1, which is characteristic of visceral obesity, angiotensinogen II independently or indirectly stimulate the activation of NTP-κB, which provokes endothelial dysfunction, an inflammatory cascade of cytokines, the formation of oxidative stress in the vascular wall, leading to the formation of atherosclerotic changes and the development of insulin resistance. The only protective factor - adiponectin - in addition to reducing its quantity and activity in visceral obesity, is suppressed by the action of a number of cytokines (see diagram).

Thus, the disorders that accompany visceral obesity are interconnected with each other like links in a “vicious circle”, when an unfavorable change in one can lead to aggravation of the other, and ultimately to the development of metabolic syndrome.

OBESITY AND METABOLISM 1 "2004

OBESITY AND METABOLISM 1 "2004

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2 years ago

Today, overweight for the majority of the population of our planet is problem No. 1. Most often this is due to the constitution of the body. In most cases, this problem can be solved with the help of two weapons - exercise and diet. But what to do if doctors diagnose visceral obesity? Let's discuss it in today's article.

Obesity is not a simple problem, but a real disease that requires treatment with the participation of specialized doctors. Visceral obesity is more common in women than in members of the opposite sex. Although visceral obesity in men is a real scourge of our century.

Many people jokingly call their stomach a bundle of nerves. And this has a scientific name - android obesity. The figure is shaped like an apple. If fat deposits accumulate in the femoral-gluteal region, then we are talking about gynoid obesity.

In medical practice, there are several degrees of obesity. To determine the degree, it is necessary to calculate the coefficient using a special formula.

What is visceral obesity? You will be surprised, but a person may not even suspect the presence of this disease, since his body weight does not change. We are talking about such a pathology when internal organs become overgrown with adipose tissue. They seem to be in a ring.

On a note! The liver and heart are the first to be targeted by visceral obesity.

We are looking for a reason

The appearance of adipose tissue on internal organs can cause both banal overeating and a sedentary lifestyle. If this is the only reason, the chances of success in treatment are enormous. But there are other reasons that need to be addressed. And in most cases, as practice shows, you cannot do without the help of a specialized doctor.

The reasons for the appearance of visceral fat include:

• genetic predisposition;
• hormonal imbalance;
• frequent drinking of beer;
• constant experience of stressful situations;
• psychoses;
• lack of motor activity;
• disturbances in the functioning of the endocrine system;
• binge eating;
• the presence of a large amount of fats and carbohydrates in the menu.

Please note that visceral obesity can result from taking a number of medications, including antidepressants.

Alarm bells of the body

As already mentioned, visceral obesity is not always accompanied by excess body weight gain, especially if the disease progresses against the background of another disease or dysfunction of the organs of the human body.

The liver, heart muscle, kidneys and pancreas are the first to be affected. As adipose tissue grows, the functioning of these organs is disrupted. Fat seems to squeeze vital organs into a ring.

Visceral obesity is accompanied by the following symptoms:

• shortness of breath;
• hypertension;
• puffiness;
• diabetes mellitus;
• frigidity;
• impotence;
• lethargy;
• pathological weakness;
• uncontrolled appetite;
• fast fatigue;
• pain in the right side of the peritoneum;
• heart rhythm disturbances;
• ischemia;
• attacks of nausea;
• depressive state.

If such symptoms occur, you should immediately contact a specialized doctor. Visceral obesity often occurs due to hormonal imbalance. Most often this happens during menopause or pregnancy.

On a note! Without obvious signs of obesity, the presence of visceral fat can be diagnosed through a CT scan.

After conducting a comprehensive examination and determining an accurate diagnosis, the doctor and patient begin to work together. The ultimate goal is weight loss and improved well-being. If visceral fat appears as a result of banal overeating, then a diet is first prescribed. With visceral obesity, the diet will be meager, but balanced.

Important! Depending on the initial fat mass, the diet can last from a couple of months to six months. After this, you should consolidate the achieved result for another 6 months so as not to gain weight in the future.

Of course, the specialist individually develops a dietary diet in each case. No favorite goodies, fast food or other foods that clog our body. From now on, only healthy and proper nutrition.

If you want to eliminate the internal fat that envelops the organs, you will have to reduce the amount of carbohydrates and fats you consume. In general, the daily calorie content of food should be much less than the total energy expended.

The process of losing weight is hampered by swelling. To normalize the removal of fluid from the body, you will have to minimize the amount of salt consumed. Granulated sugar is on the list of prohibited products. It is better to replace this sweetness with a natural beekeeping product - honey.

On a note! Have fasting days once a week. This way you can activate metabolic processes and fat burning with greater power.

As medical practice shows, if you follow a diet and exercise regularly, results will become noticeable after the first two weeks. In the future, excess weight will melt like snow under the spring sun.

But if conservative treatment is unsuccessful, specialized doctors prescribe medications whose action is aimed at blocking fat absorption. These include:

• "Glucophage";
• Orlistat.

Important! It is highly undesirable to take dietary supplements or alternative medicines that cause a false feeling of fullness or suppress appetite. This must be agreed with the treating specialist.

It is extremely rare that visceral fat is treated through surgery. The patient may be indicated for surgery to reduce the stomach and install balloons that accumulate fat.

A problem that is more typical for residents of developed countries, but has not escaped ours, is excess weight. This disease affects people of all age groups: both adult men and women, and children. But in representatives of different sexes it does not proceed in the same way. For women, gluteal-femoral fat deposition is more typical, while in men, even grade 1 obesity (initial stage) is determined mainly by an increase in waist circumference. What is the reason for the appearance of male excess weight of the first degree, how does the pathology proceed, what influences it, let’s look at it so that we can better understand what tactics to develop to combat this disease.

Common causes of the disease

The vast majority of men usually experience intense physical activity, work more and harder, but at the same time eat less flour and sweets. And yet they suffer from obesity on a par with the female sex. Why is this happening? The causes of male obesity lie in the hormonal sphere; to be more precise, there is a direct connection with the lack of the male hormone - testosterone. If the male body has enough testosterone, then the body weight of men is considered satisfactory, they feel fit, slim, they have muscles of impressive size, etc. When testosterone levels begin to fall, metabolic processes begin to fall more strongly under the influence of female sex hormones - estrogens, which men also have, but not in such significant quantities.

Estrogens in the body of men cause such an effect in metabolic processes as fat deposition. Gradually, the circle closes: in the abdominal cavity, androgen is converted into estrogen, and here the substance leptin is still produced, which blocks the formation of testicular androgen. And the process of fat deposition accelerates more and more. Without a doubt, ill-conceived nutrition, problems with the functions of the digestive tract, and physical inactivity help to accumulate excess weight. Such a common male habit as drinking beer invariably causes irreversible changes in weight. Nevertheless, disturbances in the hormonal system in men are considered to be the impetus for the development of the disease.

Diagnosis and types of disease

Measuring a man's waist circumference is sufficient reason to make a diagnosis. If the waist circumference exceeds 94 cm, then there is evidence of excess weight. A parameter of 102 cm is equal to the 2nd degree of obesity in males and is 100% proof that a man’s testosterone level is reduced. The stage of obesity in men is also determined by simple arithmetic: by calculating the body mass index (BMI). BMI is calculated by dividing body weight by its height, which is first squared. Normal body weight is considered when the BMI corresponds to a value of 18.5-25.0. With a BMI of 25.0-29.9, weight is considered overweight. Grade 1 characterizes a BMI in the range from 30.0 to 35.0. 35.0-39.0 - 2nd degree, 40 and above - 3rd degree (morbid obesity). Outwardly it looks a little different than that of the fair sex. The fat of the stronger sex chooses its location to be the waist area, thus forming a “beer belly”, sometimes making a man’s figure look like the shape of an apple.

You can compare the type of figures of different sexes by comparing 2 photographs. It is this feature of the male figure that causes the greatest harm to health. Excess fat in the body is distributed and stored in different ways. Based on the individual characteristics of the constitution and body, there are 2 types of obesity - peripheral and central. With peripheral distribution, fat accumulation occurs mainly in the tissue under the skin, and in central distribution, its accumulation occurs on the surface of internal organs.

Pitfalls of excess body weight

Since men are more likely to accumulate fat in the abdominal area, they are more likely to develop visceral obesity. Often, a predisposition to it is caused by congenital or genetic factors, nutritional disorders, and a love of consuming foods high in calories and containing sugar. What is this type of obesity and what dangers does it pose?

The visceral type forms an excess layer of fat around the heart, which puts pressure on the vital organ. As a result, the heart refuses to work as usual. As a result, arrhythmia, hypertension, shortness of breath, and increased fatigue appear. Fatty deposits surrounding the lungs prevent them from expanding fully. The patient begins to have difficulty breathing. The brain does not receive oxygen in the required volume and oxygen starvation occurs. The result is shortness of breath all the time, increased fatigue, and regular weakness. The spread of a layer of fat around the abdominal organs prevents them from functioning according to a similar principle.

In the body, metabolic processes are disrupted, diabetes mellitus, chronic gastritis, cholecystitis, and biliary dyskinesia develop. The prognosis for visceral obesity is not the most comforting - infertility and impotence. Obesity makes no exception for anyone: the consequences are unpleasant for everyone - both men and women.

Diagnosis of visceral type

There are different ways to conduct an examination in men of the visceral type. First option: measure your waist circumference. If a man's waist circumference is less than 94 cm, this is still normal. If the indicator is more than 94 and less than 101 cm, all the symptoms of excess weight are present and you should be especially careful about your health. An indicator above 102 cm gives every reason to immediately seek advice from a clinic.

Indices have been developed to calculate the degree of accumulation of fat mass around internal organs.

1. WHR - the norm is less than 1. It is the ratio of waist and hips.
2. WTR is the norm less than 1.7. The ratio of waist measurements to hip measurements. The thigh circumference is measured in the upper third part of it.
3. WAR is less than 2.4 (normal). The ratio of waist circumference to arm circumference in the middle part of the shoulder, where the biceps is at its maximum volume.
4. WhtR—the norm is less than 0.5. The ratio of waist size and height.

How to cope with such a difficult situation?

Of course, coping with stage 1 excess body weight in men is much easier than doing it in subsequent stages. But being alone is not as easy as it seems. Therefore, the advice received at an appointment with a specialist will be very valuable. After a conversation with the doctor, it will become much clearer how far the situation has gone and what the treatment tactics will be.

In any case, a man will have to change his diet. In this case, the nutritionist analyzes the food diary. The word “diet” does not sound very correct in this case, since a diet always involves a selected nutrition option for a certain period of time in order to obtain the desired result in weight and then it ends.

The entire diet of the day should be changed. Food products, indicating their quantity, must undergo a thorough analysis, after which fried foods, alcoholic drinks (especially beer), fatty foods, and sweets are removed from the list. Instead of excluded dishes, more liquid food (soups), fruits and vegetables, mainly fresh, and dietary poultry are introduced.

It is important to provide for an increase in physical activity. If shortness of breath is too strong and it is impossible to go to the gym, you should get into the habit of daily walks, which need to be increased from time to time both in time and in distance.

Walking should take from half an hour to 40 minutes a day, then it will give a positive result. If the patient decides to train in the gym, then, together with the trainer, he should select a proportionate load for the body with the possibility of its subsequent increase. In this case, the muscles will have time to grow, and the least amount of overload will be placed on the body.

As the patient’s body weight increases, the heart and vascular system, as well as the respiratory system, begin to take on loads above normal. And it takes time to reduce the layer of fat around them. To achieve significant weight loss, weight loss medications are sometimes prescribed. Group 1 of drugs (appetite suppressants): denfluramine, sibutramine, fluoxetine. They are prescribed exclusively by the attending physician due to the presence of side effects and a list of contraindications and are prescribed in life-threatening cases. Group 2 medications are substances that are designed to slow down the absorption of nutrients in the intestinal space. Xenical counteracts the absorption of fats. Acarbose eliminates the production of enzymes to break down starch, resulting in a small amount of carbohydrates entering the bloodstream.

Traditional methods for reducing appetite can also be successfully used to reduce food cravings. Teas from various plants are good for reducing appetite.

You can use the following preparation method: chamomile, birch buds, St. John's wort and immortelle in the same ratio are poured with boiling water and drunk 2-3 times a day. If a person has thought deeply and decided to get rid of excess weight once and for all, then the main commandment in such a situation is a long-term and complex combination of various techniques and techniques for weight loss with proper nutrition and leading an active lifestyle. The process may not be as fast as we would like.

However, all the efforts made will return many times over in the form of good physical shape and increased performance for many years.

Health and success!