Diabetes mellitus type 2 pathogenesis and treatment. Basic Research

Diabetes mellitus is a pathological condition in which relative or absolute insulin deficiency develops, leading to such phenomena as hyperglycemia and glucosuria. The disease is accompanied by severe disorders metabolic processes, and the frequent development of complications. For proper treatment This disease is important to understand the causes of its occurrence, as well as the mechanisms of development. Therefore, if such a diagnosis is made, as the etiology of the pathogenesis of the clinic, the treatment is interconnected.

The role of the pancreas in glucose metabolism

Etiology and pathogenesis diabetes can be better understood by considering the features carbohydrate metabolism in the human body, and what role the active substances secreted by the pancreas play in it.

The pancreas, or pancreas, is an organ with exocrine and endocrine activity. It got its name due to the fact that it is located behind the stomach. Many vessels and nerves pass through the pancreas.

The endocrine part of the organ is represented by the islets of Langerhans, which in a normal person make up from 1 to 3% of the total tissue. Islets have several types of cells, including glucagon-producing alpha cells and insulin-producing beta cells.

In the 20s of the last century, scientists isolated insulin, and this was a big breakthrough in the treatment of diabetes, since before that such patients simply died. It was found that the active substance in the form of insulin, under the influence of biochemical processes, arises from its predecessor, proinsulin, by cleaving the C-peptide from it. As a result, the same amount of both substances enters the blood. This formed the basis for the laboratory determination of C-peptide as an indicator of the ability of beta cells to produce insulin.

Not so long ago, scientists determined that the C-peptide also has a certain degree of activity and is involved in the following processes:

Decreased glycated hemoglobin.

Stimulation of glucose uptake by muscle tissue.

Decrease in insulin resistance, and thereby enhance the effects of insulin.

Reducing the likelihood of developing neuropathy.

Improves the filtration work of the kidneys and strengthens the retina.

The body normally needs to release about 50 IU of insulin per day. Pancreas in the normal state of the organ has from 150 to 250 units. The secreted insulin enters the hepatocytes through the portal vein system. There it undergoes partial inactivation with the participation of the insulinase enzyme. The remaining active part of the substance binds to proteins, and in a certain amount remains in an unbound form. The proportions of bound and free insulin are regulated depending on the amount of sugar in the blood. Free insulin is normally formed intensively during hyperglycemia.

In addition to the liver, insulin breaks down in the kidneys, adipose tissue, muscles and placenta. The formation of this hormone normally depends on the level of glucose, for example, with an excess of sweets in the food consumed, it causes an increased work of insulin-producing cells. The decrease and increase in insulin in the blood can be caused by other factors and hormonal substances, but the main regulation depends on the intake of sugars from food.

How insulin works

In a disease such as diabetes mellitus, the etiology of pathogenesis lies in certain factors that contribute to the disruption of insulin production, or the lack of response of peripheral tissues to its action.

On the cells of some tissues there are a special type of receptors through which the transfer of glucose is carried out. Insulin joins them and speeds up the absorption process by 20-40 times.

Etiology and pathogenesis of diabetes mellitus

Diabetes mellitus, according to the classification, is divided into types 1 and 2 (insulin-dependent and non-insulin dependent). There are also other types of diseases - gestational (during pregnancy), some specific conditions, genetic defects that cause a violation of sugar metabolism. Diabetes is noted separately, which develops as a result of other endocrine pathologies (thyrotoxicosis, Cushing's syndrome, etc.), a disease as a result of exposure to pharmacological and chemical substances, some syndromes that may be accompanied by diabetes mellitus (Down, Friedreich, etc.).

The main are the first two types of the disease, each of which has its own characteristics of development and causes.

Etiology of type 1 diabetes

Insulin-dependent diabetes mellitus is considered an autoimmune disease in which beta cells located in the pancreas are damaged. Their main function is to produce insulin. With type 1 diabetes, there is a decrease or cessation of its production and the development of absolute insulin deficiency. It is noted in young people with a rapid development of clinical symptoms.

The development of this variant of the disease is associated with hereditary predisposition. However, confirmation of this appears only in a third of patients. In this case, antibodies to glutamate decarboxylase, beta cells, or directly to insulin are detected. And this is the main proof of the autoimmune process.

A high probability of manifestation of the disease exists in the presence of other autoimmune pathologies, both associated with endocrine organs (Addison's disease, autoimmune thyroiditis) and others (Crohn's disease, rheumatism, vitiligo).

The pathogenesis of type 1 diabetes

If there is a predisposition to this type of disease, after the appearance of a situation that starts the process, type 1 diabetes develops. These mechanisms are:

Viral, bacterial or fungal infection;

Stressful situation;

Violation of the regimen and quality of food intake;

Intoxication of non-infectious origin (including the use of certain drugs);

Irradiation.

Under the influence of the trigger mechanism, antibodies begin to be intensively produced, in the initial stage, insulin production remains within the normal range. In a disease such as type 1 diabetes mellitus, pathogenesis is characterized by the onset of a massive destruction of beta cells due to the aggressive influence of the patient's own antibodies. But even in this case, for some time the level of glucose in the blood does not change. The strengthening of the autoimmune reaction is also due to the fact that under the influence of diabetogenic factors, an increase in the number of free radicals. They lead to an increase in the process of damage to beta cells.

Clinical manifestations, which determine the pathogenesis of the main symptoms of diabetes mellitus, begin to develop when about 80-90% of insulin-producing cells die. In such patients, insulin administration is vital to prevent the development of hyperglycemia, ketoacidosis and death.

Type 2 diabetes mellitus etiology

The non-insulin-dependent form of diabetes is determined by metabolic disorders with the development of insensitivity of tissue receptors to insulin and a change in one degree or another in the work of beta cells. It is detected mainly in people of middle and senile age, the increase in symptoms occurs more slowly than in the insulin-dependent type of the disease.
The etiology of type 2 diabetes mellitus is that against the background of a hereditary tendency to develop and under the influence of eating disorders, overeating, weight gain, stressful situations, as well as as a result of malnutrition in the womb and in the first year after birth, a metabolic disorder develops. glucose.

The pathogenesis of type 2 diabetes

Current data suggest that the pathogenesis of type 2 diabetes mellitus is an increase in insulin resistance in peripheral tissues, which most often occurs with abdominal obesity and impaired functioning of pancreatic cells that produce insulin. When a disease such as diabetes mellitus is detected in children, the pathogenesis and causes of such a disease are no different from those in adults. A feature of the disease in childhood is that they predominantly develop type 1 diabetes, and the course is much more severe than in patients of mature years.

Insulin resistance is hepatic and peripheral. When switching to replacement therapy there is a decrease in glucose production in the liver, but this treatment in no way affects insulin sensitivity from peripheral tissues.

To improve the condition in this form of diabetes in the initial stage, it is sufficient to reduce weight, increase physical activity, adherence to low-carbohydrate and low calorie diet. In the future, hypoglycemic drugs of various mechanisms of action are used, and if necessary, insulin.

For the successful treatment of diabetes mellitus, a prerequisite is the impact on all the components of its pathogenesis. Scientists have been studying the causes and mechanisms of diabetes for many years, and a number of pathophysiological processes and etiological factors have already been established that lead to hyperglycemia as a result.

What triggers diabetes

Diabetes mellitus is a heterogeneous pathology in which a complex of metabolic disorders develops. Main characteristics type 2 diabetes is insulin resistance and poor function of beta cells of varying severity.

Modern Scientific research proved that many factors are involved in the development of diabetes mellitus and a significant role in the development this disease played by external, non-genetic factors.

It has now been proven that the following factors play a major role in the pathogenesis of type 2 diabetes:

• hereditary predisposition - diabetes mellitus in parents, close relatives;
• wrong way of life bad habits, low degree of physical activity, chronic fatigue, frequent stress;
• food - high-calorie and leading to obesity;
• insulin resistance - a violation of the metabolic response to insulin;
• violation of insulin production and increased production of glucose by the liver.

The role of individual etiological factors in the pathogenesis of diabetes

The pathogenesis of diabetes mellitus depends on the type. In type 2 diabetes, it includes hereditary and external factors. In fact, genetic factors are more important in type 2 diabetes than in type 1 diabetes. This conclusion is based on a study of twins.

It used to be thought that identical (monozygous) twins had an incidence of type 2 diabetes of about 90-100%.

However, with the use of new approaches and methods, it has been proven that concordance (coincidence in the presence of the disease) in monozygotic twins is slightly lower, although it remains quite high 70-90%. This indicates a significant contribution of heredity in the predisposition to type 2 diabetes.

Genetic predisposition is important in the development of prediabetes (impaired glucose tolerance). Whether a person develops diabetes further depends on their lifestyle, diet, and other external factors.

The role of obesity and physical inactivity

Frequent overeating and a sedentary lifestyle lead to obesity and further exacerbate insulin resistance. This contributes to the implementation of the genes responsible for the development of type 2 diabetes.

Obesity, especially abdominal, plays a special role not only in the pathogenesis of insulin resistance and resulting metabolic disorders, but also in the pathogenesis of type 2 diabetes.

This is because visceral adipocytes, in contrast to subcutaneous adipose tissue adipocytes, are less sensitive to the anti-lipolytic action of the hormone insulin and more sensitive to the lipolytic action of catecholamines.

This circumstance causes the activation of lipolysis of the visceral fat layer and the entry, first into the bloodstream of the portal vein, and then into the systemic circulation, of a large amount of free fatty acids. In contrast, the cells of the subcutaneous fat layer to slow down the action of insulin, it promotes the reesterification of free fatty acids to triglycerides.

Insulin resistance of skeletal muscles lies in the fact that they predominantly utilize free fatty acids at rest. This prevents myocytes from utilizing glucose and leads to an increase in blood sugar and a compensatory increase in insulin. Moreover, fatty acids do not allow insulin to bind to hepatocytes, and this exacerbates insulin resistance at the liver level and inhibits the inhibitory effect of the hormone on gluconeogenesis in the liver. Gluconeogenesis leads to a constant increased production of glucose in the liver.

Thus, a vicious circle is created - an increase in the level of fatty acids causes even greater insulin resistance of muscle, adipose and liver tissue. It also leads to the launch of lipolysis, hyperinsulinemia, and hence to an increase in the concentration of fatty acids.

Insufficient physical activity in type 2 diabetics exacerbates existing IR.

At rest, the transfer of glucose transporter substances (GLUT-4) in myocytes is sharply reduced. Muscle contraction during exercise increases glucose delivery to myocytes, this is due to an increase in GLUT-4 translocation to the cell membrane.

Causes of insulin resistance

Insulin resistance in type 2 diabetes mellitus is a condition in which there is an insufficient biological response of tissues to insulin at its normal concentration in the blood. In the study of genetic defects that cause the presence of insulin resistance, it was found that it mainly occurs against the background of the normal functioning of insulin receptors.

Insulin resistance is associated with insulin dysfunction at the receptor, pre-receptor and post-receptor levels. Receptor insulin resistance is associated with an insufficient number of receptors on the cell membrane, as well as a change in their structure. Prereceptor insulin resistance is caused by a disorder in the early stages of insulin secretion and (or) with a pathology of the conversion of proinsulin to C-peptide and insulin. Post-receptor insulin resistance includes a defect in the activity of transducers that signal insulin within the cell, as well as those involved in protein synthesis, glycogen, and glucose transport.

The most important consequences of insulin resistance are hyperinsulinemia, hyperglycemia and dyslipoproteinemia. In violation of insulin production, hyperglycemia plays a leading role and leads to its gradual relative deficiency. In patients with type 2 diabetes, the compensatory capacity of pancreatic beta cells is limited due to the genetic breakdown of glucokinase and the glucose transporter GLUT-2. These substances are responsible for the production of insulin for glucose stimulation.

Insulin production in type 2 diabetics

In patients with type 2 diabetes, insulin secretion is usually impaired. Namely:

• a delayed initial phase of the secretory response to intravenous glucose loading;
• reduced and delayed secretory response to the use of mixed food;
• increased levels of proinsulin and products of its processing;
• the rhythm of fluctuations in insulin secretion is disturbed.

Among possible causes disorders of insulin production can be called both primary genetic defects in beta cells, and secondary developing disorders due to lipo - and glucose toxicity. There are studies aimed at finding out other causes of impaired insulin secretion.

In the study of insulin production in patients with prediabetes, it was found that even before the increase in fasting sugar levels and with normal levels of glycosylated hemoglobin, the rhythm of fluctuations in insulin production is already disturbed. This consists in reducing the ability of pancreatic beta cells to respond with peak insulin secretion to peak fluctuations in blood glucose concentration throughout the day.

Moreover, obese patients with insulin resistance produce more insulin in response to the same amount of glucose than healthy people with normal weight and without insulin resistance. This means that in people with prediabetes, insulin secretion is already deficient, and this is important for the development of type 2 diabetes in the future.

Early stages of impaired insulin secretion

Changes in insulin secretion in prediabetes occur due to increased concentrations of free fatty acids. This, in turn, leads to inhibition of pyruvate dehydrogenase, and hence to a slowdown in glycolysis. Inhibition of glycolysis leads in beta cells to a decrease in the formation of ATP, which is the main trigger for insulin secretion. A role for glucose toxicity in a defect in insulin secretion in prediabetic patients (impaired glucose tolerance) is ruled out because hyperglycemia has not yet been observed.

Glucose toxicity is a set of bimolecular processes in which prolonged excess concentration of glucose in the blood leads to damage to insulin secretion and tissue sensitivity to it. This is another vicious circle in the pathogenesis of type 2 diabetes. It can be concluded that hyperglycemia is not only main symptom, but also a factor in the progression of type 2 diabetes due to the action of the phenomenon of glucose toxicity.

With prolonged hyperglycemia, a decrease in insulin secretion is observed in response to a glucose load. At the same time, the secretory response to stimulation with arginine remains, on the contrary, enhanced for a long time. All of the above problems with insulin production are corrected while maintaining a normal blood sugar concentration. This proves that the phenomenon of glucose toxicity plays an important role in the pathogenesis of defective insulin secretion in type 2 diabetes.

Also, glucose toxicity leads to a decrease in tissue sensitivity to insulin. Thus, achieving and maintaining normal indicators blood glucose will increase the sensitivity of peripheral tissues to the hormone insulin.

The pathogenesis of the main symptom

Hyperglycemia is not only a marker of diabetes, but also the most important link in the pathogenesis of type 2 diabetes.

It disrupts insulin secretion by pancreatic beta cells and glucose uptake by tissues, which aims to correct carbohydrate metabolism disorders in patients with type 2 diabetes mellitus to normoglycemia.

An increase in fasting sugar is an early symptom of type 2 diabetes, which is caused by increased sugar production by the liver. The severity of insulin secretion disorders at night directly depends on the degree of fasting hyperglycemia.

Insulin resistance of hepatocytes is not a primary breakdown, it appears as a result of the influence of metabolic and hormonal disorders, including an increase in glucagon production. In chronic hyperglycemia, beta cells lose their ability to respond to rising blood glucose levels by decreasing glucagon secretion. As a result, hepatic glycogenolysis and gluconeogenesis increase. This is one of the factors of relative insulin deficiency in the portal blood circulation.

An additional reason for the development of insulin resistance at the liver level is the inhibitory effect of fatty acids on the uptake and internalization of insulin by hepatocytes. Excessive intake of free fatty acids into the liver sharply stimulates gluconeogenesis due to an increase in the production of acetyl-CoA in the Krebs cycle.

Moreover, acetyl-CoA, in turn, reduces the activity of the enzyme pyruvate dehydrogenase. The result of this is excess secretion of lactate in the Cori cycle (lactate is one of the main products for gluconeogenesis). Fatty acids also inhibit the activity of the glycogen synthase enzyme.

Role in the pathogenesis of type 2 diabetes mellitus amylin and leptin

Recently, the substances amylin and leptin play a significant role in the mechanism of development of type 2 diabetes. The role of amylin was established only 15 years ago. Amylin is an islet amyloid polypeptide that resides in the secretory granules of beta cells and is normally produced together with insulin in a ratio of approximately 1:100. The content of this substance is increased in patients with insulin resistance and impaired carbohydrate tolerance (prediabetes).

In type 2 diabetes, amylin accumulates in the islets of Langerhans as amyloid. It is involved in the regulation of carbohydrate metabolism by adjusting the rate of absorption of glucose from the intestines, and inhibiting the production of insulin in response to glucose irritation.

In the last 10 years, the role of leptin in the pathology of fat metabolism and the development of type 2 diabetes has been studied. Leptin is a polypeptide produced by white adipose tissue cells and acts on the nucleus of the hypothalamus. Namely, on the ventro-lateral nuclei responsible for eating behavior.

Leptin secretion decreases during fasting and increases during obesity, in other words, it is regulated by the adipose tissue itself. A positive energy balance is associated with an increase in the production of leptin and insulin. The latter interact with the hypothalamic centers, most likely through the secretion of the hypothalamic neuropeptide Y.

Fasting leads to a decrease in the amount of adipose tissue and a decrease in the concentration of leptin and insulin, which stimulates the secretion of hypothalamic neuropeptide Y by the hypothalamus. nervous system.

Both relative and absolute insufficiency of leptin leads to an increase in the secretion of neuropeptide Y, and hence to the development of obesity. With an absolute deficiency of leptin, its exogenous administration, in parallel with a decrease in appetite and weight, reduces the content of mRNA that encodes neuropeptide Y. Exogenous administration of leptin with its relative deficiency (as a result of a mutation of the gene that encodes its receptor) does not affect weight.

It can be assumed that the absolute or relative deficiency of leptin leads to the loss of inhibitory control over the secretion of the hypothalamic neuropeptide Y. This is accompanied by autonomic and neuroendocrine pathologies that are involved in the development of obesity.

The pathogenesis of type 2 diabetes is a very complex process. It plays a major role in insulin resistance, violation of insulin production and chronic increased secretion of glucose by the liver. When selecting treatment to achieve compensation for type 2 diabetes and prevent complications, this should be taken into account.

Non-insulin dependent diabetes (NIDDM, type 2 diabetes)- a heterogeneous disease characterized by a violation of insulin secretion and sensitivity of peripheral tissues to insulin (insulin resistance).

Etiology of NIDDM:

1) heredity- defective genes (on chromosome 11 - a violation of insulin secretion, on chromosome 12 - a violation of the synthesis of insulin receptors, genetic defects in the glucose recognition system by β-cells or peripheral tissues), transmitted by a dominant pathway; both identical twins develop NIDDM in 95-100% of cases.

2) overnutrition and obesity- high-calorie foods with a large amount of easily absorbed carbohydrates, sweets, alcohol and a deficiency of vegetable fiber, together with a sedentary lifestyle, contribute to impaired insulin secretion and the development of insulin resistance

Pathogenesis of NIDDM caused by violations at three levels:

1. Violation of insulin secretion- the first key defect in NIDDM, detected both at the earliest and at the most pronounced stages of the disease:

A) quality problems- with NIDDM, the content of insulin in the blood on an empty stomach is significantly reduced, proinsulin prevails

B) kinetic disturbances– in healthy people, in response to glucose administration, two-phase insulin secretion is observed: the first secretion peak begins immediately after stimulation with glucose, ends by the 10th minute, due to the release of stored insulin from β-cell granules; the second peak of secretion begins after 10 min. with a / in the introduction or after 30 minutes. or later after oral intake glucose, prolonged, reflects the secretion of newly synthesized insulin in response to stimulation of β-cells with glucose; with NIDDM there is no first phase and the second phase of insulin secretion is smoothed out

C) quantitative violations- NIDDM is characterized by severe insulinopenia, due to a decrease in the mass of β-cells of the islets of Langvrhans, deposition of amyloid deposits in the islets (synthesized from amylin, which is secreted by β-cells along with insulin and participates in the conversion of proinsulin to insulin), "glucose toxicity" (chronic hyperglycemia causes structural disorders of the islets of Langerhans and decreased insulin secretion), etc.

2. Insulin resistance of peripheral tissues:

A) prereceptor- associated with genetically determined production of altered, inactive

Molecules of insulin or incomplete conversion of proinsulin to insulin

B) receptor- associated with a decrease in the number of active insulin receptors, the synthesis of abnormally inactive receptors, the appearance of anti-receptor antibodies.

B) post-receptor- a decrease in the activity of insulin receptor tyrosine kinase, a decrease in the number of glucose transporters (proteins on the inner surface of the cell membrane that ensure the transport of glucose inside the cell),

In the development of insulin resistance, the circulation of insulin antagonists in the blood (AT to insulin, contrainsular hormones: somatotropin, cortisol, thyroid hormones, thyrotropin, prolactin, glucagon, KA) is also important.

3. Increased production of glucose by the liver- due to increased gluconeogenesis, suppression of glucose production by the liver, disruption of the circadian rhythm of glucose formation (no decrease in glucose production at night), etc.

Clinical manifestations of NIDDM:

1. The following complaints are subjectively characteristic:

- severe general and muscle weakness (due to a lack of energy, glycogen and protein in the muscles)

- thirst - in the period of decompensation of diabetes, patients can drink 3-5 liters or more per day; the higher the hyperglycemia, the more pronounced the thirst; dry mouth (due to dehydration and reduced function salivary glands)

- frequent and profuse urination both day and night

- obesity - often, but not always

- increased appetite

- itching of the skin - especially in women in the genital area

2. Objectively state of organs and systems:

A) skin:

– dry skin, decreased turgor and elasticity

- pustular skin lesions, recurrent furunculosis, hydroadenitis, epidermophytosis of the feet

- xanthomas of the skin (papules and nodules of yellowish color, filled with lipids, located in the buttocks, legs, knee and elbow joints, forearms) and xanthelasma (yellow lipid spots on the skin of the eyelids)

- rubeosis - expansion of skin capillaries with hyperemia of the skin in the cheekbones and cheeks (diabetic blush)

- lipoid necrobiosis of the skin - more often on the legs; at first, dense reddish-brown or yellowish nodules or spots appear, surrounded by an erythematous border of dilated capillaries; the skin above them gradually atrophies, becomes smooth, shiny, with pronounced lichenification (“parchment”); sometimes the affected areas ulcerate, heal very slowly, leaving behind areas of pigmentation

B) digestive system:

- progressive caries

- periodontal disease, loosening and loss of teeth

- alveolar pyorrhea, gingivitis, ulcerative or aphthous stomatitis

– chronic gastritis, duodenitis with the gradual development of atrophy, a decrease in the secretion of gastric juice;

Decreased motor function of the stomach up to gastroparesis

- bowel dysfunction: diarrhea, steatorrhea, malabsorption syndrome

– fatty hepatosis of the liver, chronic calculous cholecystitis, dyskinesia of the gallbladder, etc.

B) cardiovascular system:

– early development atherosclerosis and coronary artery disease with various complications (MI with diabetes can proceed without pain - parishioner's cardiac hypoesthesia syndrome, more often transmural, severe, accompanied by various complications)

– arterial hypertension(often secondary due to nephroangiopathy, atherosclerosis renal arteries and etc.)

- "diabetic heart" - dysmetabolic myocardial dystrophy

G) respiratory system:

- susceptibility to pulmonary tuberculosis severe course, frequent exacerbations, complications

– frequent pneumonia (due to microangiopathies of the lungs)

– frequent acute bronchitis and predisposition to develop chronic bronchitis

D) urinary system: predisposition to infectious and inflammatory diseases urinary tract(cystitis, pyelonephritis), etc.

Diagnosis of NIDDM: see question 74.

Treatment for NIDDM:

1. Diet– must meet the following requirements:

- be physiological in composition and ratio of the main ingredients (60% carbohydrates, 24% fats, 16% proteins), covering all energy costs depending on the degree of physical activity and ensuring the maintenance of a normal "ideal" body weight; with an excess of body weight, a hypocaloric diet is indicated at the rate of 20-25 kcal per 1 kg of body weight / day

- 4-5 meals a day with the following distribution between daily calorie intake: 30% for breakfast, 40% for lunch, 10% for afternoon tea, 20% for dinner

- exclude easily digestible carbohydrates, alcohol intake, increase the content of vegetable fiber

- limit fats of animal origin (40-50% of fats should be vegetable)

A diet in the form of monotherapy is carried out until, against the background of its use, it is possible to maintain full compensation for diabetes mellitus.

2. Weight loss, adequate exercise(with excess body weight, it is possible to use anorectics - the drug of central action is optimal, which inhibits the reuptake of catecholamines, meridia (sibutramine) 10 mg 1 time / day, for 1 month weight loss 3-5 kg)

3. Medical therapy - oral hypoglycemic drugs (and in patients with an insulin-requiring form of type 2 diabetes + insulin therapy with mixed drugs of combined action: mixtard-30, humulin profile-3, insuman comb-25 GT in the mode of two injections before breakfast and dinner):

A) secretogens- drugs that stimulate the secretion of ready-made insulin by b-cells:

1) sulfonylurea derivatives - chlorpropamide (I generation) 250 mg / day in 1 or 2 doses; glibenclamide (maninil) 1.25-20 mg/day, including micronized forms of maninil 1.75 and 3.5; glipizide, gliclazide (diabeton) 80-320 mg/day, gliquidone, glimepiride (amaril) 1-8 mg/day

2) derivatives of amino acids - optimal for the regulation of postprandial hyperglycemia: Novonorm (repaglinide) 0.5-2 mg before meals up to 6-8 mg / day, starlix (nateglinide)

B) biguanides- increase in the presence of insulin the peripheral utilization of glucose, reduce gluconeogenesis, increase the utilization of glucose by the intestines with a decrease in the level of glycemia of the blood flowing from the intestines: N, N-dimethylbiguanide (siofor, metformin, glucophage) 500-850 mg 2 times / day

B) inhibitorsA-glucosidase- reduce the absorption of carbohydrates in the gastrointestinal tract: glucobay (acarbose) 150-300 mg / day in 3 doses with meals

D) glitazones (thiosalidinediones, insulin sensitizers)- increase the sensitivity of peripheral tissues to insulin: actos (pioglitazone) 30 mg 1 time / day

4. Prevention and treatment late complications NIDSD– for successful solution of the problem it is necessary:

a) compensate for carbohydrate metabolism disorders up to normoglycemia, aglucosuria by adequate and correct treatment of NIDDM

b) compensate for fat metabolism with appropriate lipid-lowering therapy: diet with fat restriction, drugs (statins, fibrates, drugs nicotinic acid and etc.)

c) provide normal level AD (antihypertensive drugs, especially ACE inhibitors, which additionally have a nephroprotective effect)

d) to ensure the balance of the coagulation and anticoagulation systems of the blood

Prevention of late complications includes Preservation of stable compensation of carbohydrate metabolism for a long time and early detection of the initial stages of late complications of diabetes:

1) diabetic retinopathy- it is necessary to regularly conduct an examination of the fundus of the eye once a year for the first 5 years, and then once every 6 months; with neoplasm of retinal vessels, laser coagulation is indicated

2) diabetic nephropathy- it is necessary to determine microalbuminuria once every 6 months; with the appearance of signs of chronic renal failure - a diet with a restriction of animal protein (up to 40 g per day) and table salt (up to 5 g per day), the use of ACE inhibitors, detoxification therapy, and with continued deterioration in kidney function - hemodialysis and other complications.

Prevention of NIDDM: a healthy lifestyle (avoid physical inactivity and obesity, do not abuse alcohol, smoking, etc., rational nutrition, avoid stress) + constant adequate correction by diet or medication for the first episodes of hyperglycemia, followed by periodic monitoring of blood sugar levels.

- is chronic endocrine disease, which develops due to insulin resistance and dysfunction of pancreatic beta cells, is characterized by a state of hyperglycemia. Manifested by profuse urination (polyuria), increased thirst (polydipsia), itching skin and mucous membranes increased appetite, hot flashes, muscle weakness. The diagnosis is based on the results laboratory research. A blood test is performed for the concentration of glucose, the level of glycosylated hemoglobin, and a glucose tolerance test. Hypoglycemic drugs, a low-carbohydrate diet, and increased physical activity are used in the treatment.

ICD-10

E11 non-insulin dependent diabetes mellitus

General information

Pathogenesis

At the heart of type 2 diabetes is a violation of carbohydrate metabolism due to increased cell resistance to insulin (insulin resistance). The ability of tissues to receive and utilize glucose decreases, a state of hyperglycemia develops - an increased level of plasma sugar, and alternative ways of obtaining energy from free fatty acids and amino acids are activated. To compensate for hyperglycemia, the body intensively removes excess glucose through the kidneys. Its amount in the urine increases, glucosuria develops. A high concentration of sugar in biological fluids causes an increase in osmotic pressure, which provokes polyuria - profuse frequent urination with loss of fluid and salts, leading to dehydration and water-electrolyte imbalance. These mechanisms explain most of the symptoms of diabetes - intense thirst, dry skin, weakness, arrhythmias.

Hyperglycemia alters the processes of peptide and lipid metabolism. Sugar residues attach to protein and fat molecules, disrupting their function, hyperproduction of glucagon occurs in the pancreas, the breakdown of fats as an energy source is activated, glucose reabsorption by the kidneys increases, transmitter transmission in the nervous system is disrupted, and intestinal tissues become inflamed. Thus, the pathogenetic mechanisms of DM provoke vascular pathologies (angiopathy), the nervous system (neuropathy), digestive system, glands of endocrine secretion. A later pathogenetic mechanism is insulin deficiency. It is formed gradually, over several years, due to depletion and natural programmed death of β-cells. Over time, a moderate deficiency of insulin is replaced by a pronounced one. Secondary insulin dependence develops, patients are prescribed insulin therapy.

Classification

Depending on the severity of carbohydrate metabolism disorders in diabetes mellitus, a compensation phase is distinguished (a state of normoglycemia is reached), a subcompensation phase (with a periodic increase in blood glucose levels) and a decompensation phase (hyperglycemia is stable, difficult to correct). Depending on the severity, there are three forms of the disease:

1. Light. Compensation is achieved by adjusting nutrition or diet in combination with a minimum dosage of a hypoglycemic drug. The risk of complications is low.
2. Average. To compensate for metabolic disorders, regular intake of hypoglycemic agents is necessary. The probability of the initial stages of vascular complications is high.
3. Heavy. Patients need constant use of tableted hypoglycemic drugs and insulin, sometimes only insulin therapy. Serious diabetic complications are formed - angiopathy of small and large vessels, neuropathy, encephalopathy.

Symptoms of type 2 diabetes

The disease develops slowly, at the initial stage, the manifestations are barely noticeable, which greatly complicates the diagnosis. The first symptom is an increased feeling of thirst. Patients feel dry mouth, drink up to 3-5 liters per day. Accordingly, the amount of urine and the frequency of the urge to empty Bladder. Children may develop enuresis, especially at night. Due to frequent urination and high sugar content in the excreted urine, the skin of the inguinal region is irritated, itching occurs, and redness appears. Gradually, itching covers the abdomen, armpits, bends of the elbows and knees. Insufficient supply of glucose to the tissues contributes to an increase in appetite, patients experience hunger already 1-2 hours after eating. Despite the increase in the caloric content of the diet, the weight remains the same or decreases, since glucose is not absorbed, but is lost with urine.

Additional symptoms are fatigue, constant feeling fatigue, daytime sleepiness, weakness. The skin becomes dry, thinner, prone to rashes, fungal infections. The body bruises easily. Wounds and abrasions heal for a long time, often become infected. Girls and women develop genital candidiasis, boys and men develop urinary tract infections. Most patients report a tingling sensation in the fingers, numbness in the feet. After eating, you may experience nausea and even vomiting. Arterial pressure increased, frequent headaches and dizziness.

Complications

The decompensated course of type 2 diabetes is accompanied by the development of acute and chronic complications. Acute conditions are those that occur quickly, suddenly and are accompanied by a risk lethal outcome- hyperglycemic coma, lactic acid coma and hypoglycemic coma. Chronic complications form gradually, include diabetic micro- and macroangiopathies, manifested by retinopathy, nephropathy, thrombosis, and vascular atherosclerosis. Diabetic polyneuropathies are detected, namely polyneuritis peripheral nerves, paresis, paralysis, autonomic disturbances in work internal organs. There are diabetic arthropathy - joint pain, limited mobility, a decrease in the volume of synovial fluid, as well as diabetic encephalopathy - mental disorders, manifested by depression, emotional instability.

Diagnostics

The difficulty of identifying non-insulin-dependent diabetes mellitus is due to the absence of severe symptoms on initial stages diseases. In this regard, people at risk and all persons over 40 years of age are recommended screening plasma tests for sugar levels. Laboratory diagnostics is the most informative, it allows you to detect not only the early stage of diabetes, but also the state of pre-diabetes - a decrease in glucose tolerance, manifested by prolonged hyperglycemia after a carbohydrate load. With signs of diabetes, an examination is carried out by an endocrinologist. Diagnosis begins with the clarification of complaints and the collection of anamnesis, the specialist clarifies the presence of risk factors (obesity, physical inactivity, hereditary burden), reveals the basic symptoms - polyuria, polydipsia, increased appetite. The diagnosis is confirmed after receiving the results laboratory diagnostics. Specific tests include:

• Fasting glucose. The criterion for the disease is a glucose level above 7 mmol / l (for venous blood). The material is taken after 8-12 hours of fasting.
• Glucose tolerance test. To diagnose diabetes at an early stage, the concentration of glucose is examined a couple of hours after eating carbohydrate foods. An indicator above 11.1 mmol / l reveals diabetes, in the range of 7.8-11.0 mmol / l prediabetes is determined.
• Glycated hemoglobin. The analysis allows you to evaluate the average value of glucose concentration over the past three months. Diabetes is indicated by a value of 6.5% or more ( deoxygenated blood). With a result of 6.0-6.4%, prediabetes is diagnosed.

Differential diagnosis includes distinguishing between non-insulin-dependent diabetes mellitus and other forms of the disease, in particular, type 1 diabetes mellitus. Clinical differences are a slow increase in symptoms, a later onset of the disease (although in recent years the disease has also been diagnosed in young people 20-25 years old). Laboratory differential signs - elevated or normal levels of insulin and C-peptide, the absence of antibodies to pancreatic beta cells.

Treatment of type 2 diabetes

In practical endocrinology, a systematic approach to therapy is common. On the early stages diseases, the focus is on changing the lifestyle of patients and consultations, in which a specialist talks about diabetes, ways to control sugar. With persistent hyperglycemia, the question of the use of drug correction is decided. The full range of therapeutic measures includes:

• Diet. The main principle of nutrition is to reduce the amount of food high in fat and carbohydrates. Especially "dangerous" are products with refined sugar - confectionery, sweets, chocolate, sweet carbonated drinks. The diet of patients consists of vegetables, dairy products, meat, eggs, a moderate amount of cereals. We need a fractional diet, small portions, the rejection of alcohol and spices.
• Regular physical activity. Patients without severe diabetic complications are shown sports activities that enhance oxidation processes (aerobic exercise). Their frequency, duration and intensity are determined individually. Most patients are allowed walking, swimming and walking. The average time of one lesson is 30-60 minutes, the frequency is 3-6 times a week.
• Medical therapy. Are used medicines several groups. The use of biguanides and thiazolidinediones, drugs that reduce insulin resistance of cells, absorption of glucose in the gastrointestinal tract and its production in the liver, is common. With their insufficient effectiveness, drugs are prescribed that enhance the activity of insulin: DPP-4 inhibitors, sulfonylurea derivatives, meglitinides.

Forecast and prevention

Timely diagnosis and responsible attitude of patients to the treatment of DM make it possible to achieve a state of stable compensation, in which normoglycemia persists for a long time, and the quality of life of patients remains high. To prevent the disease, it is necessary to adhere to a balanced diet high in fiber, limiting sugary and fatty foods, and fractional meals. It is important to avoid hypodynamia, to provide the body with daily physical activity in the form of walking, to play sports 2-3 times a week. Regular glucose monitoring is necessary for people at risk ( excess weight, mature and elderly age cases of DM among relatives).

Type 2 diabetes- symptoms and treatment

What is type 2 diabetes? We will analyze the causes of occurrence, diagnosis and methods of treatment in the article of Dr. Khitaryan A. G., a phlebologist with an experience of 35 years.

Definition of disease. Causes of the disease

The epidemic of diabetes mellitus (DM) has been going on for a long time. According to the World Health Organization (WHO), in 1980 there were about 150 million people on the planet suffering from diabetes, and in 2014 - about 421 million. Unfortunately, there has not been a tendency to regress in the incidence over the past decades, and today we can safely say that DM is one of the most common and serious diseases.

Type II diabetes- a chronic non-infectious, endocrine disease, which is manifested by profound disorders of lipid, protein and carbohydrate metabolism associated with an absolute or relative deficiency of a hormone produced by the pancreas.

In patients with type II diabetes, the pancreas produces a sufficient amount of insulin, a hormone that regulates carbohydrate metabolism in the body. However, due to a violation of metabolic reactions in response to the action of insulin, a deficiency of this hormone occurs.

Insulin-dependent type II DM has a polygenic nature, and is also a hereditary disease.

The cause of this pathology is a combination of certain genes, and its development and symptoms are determined by concomitant risk factors, such as unbalanced nutrition, low physical activity, constant stressful situations, age from 40 years.

The growing pandemic of obesity and type II diabetes are closely linked and represent major global health threats in society. It is these pathologies that are the causes of the appearance chronic diseases: coronary disease heart, hypertension, and hyperlipidemia.

If you experience similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

Type 2 diabetes symptoms

Most often, the symptoms of type II diabetes are mild, so this disease can be detected thanks to the results of laboratory tests. Therefore, people belonging to the risk group (presence of obesity, high pressure, various metabolic syndromes, age from 40 years), you should undergo a routine examination to exclude or timely detect the disease.

The main symptoms of type II diabetes include:

• permanent and unmotivated weakness, drowsiness;
• constant thirst and dry mouth;
• polyuria - frequent urination;
• increased appetite (during the period of decompensation (progression and deterioration) of the disease, appetite decreases sharply);
• skin itching (in women often occurs in the perineum);
• slow healing wounds;
• blurred vision;
• limb numbness.

The period of decompensation of the disease is manifested by dry skin, a decrease in firmness and elasticity, and fungal infections. Due to abnormally elevated lipid levels, skin xanthomatosis (benign neoplasms) occurs.

In patients with type II diabetes, the nails are prone to brittleness, loss of color or the appearance of yellowness, and 0.1 - 0.3% of patients suffer from lipoid necrobiosis of the skin (deposits of fat in the destroyed areas of the collagen layer).

In addition to the symptoms of type II diabetes itself, symptoms of late complications of the disease also make themselves felt: leg ulcers, decreased vision, heart attacks, strokes, leg vascular lesions and other pathologies.

The pathogenesis of type 2 diabetes

The main cause of type II diabetes is insulin resistance(loss of cell response to insulin), due to a number of factors external environment and genetic factors, occurring against the background of dysfunction of β-cells. According to research data, with insulin resistance, the density of insulin receptors in tissues decreases and translocation (chromosomal mutation) of GLUT-4 (GLUT4) occurs.

Elevated levels of insulin in the blood hyperinsulinemia) leads to a decrease in the number of receptors on target cells. Over time, β-cells stop responding to rising glucose levels. As a result, a relative deficiency of insulin is formed, in which carbohydrate tolerance is impaired.

Insulin deficiency leads to a decrease in the utilization of glucose (sugar) in tissues, an increase in the breakdown of glycogen to glucose and the formation of sugar from non-carbohydrate components in the liver, thereby increasing glucose production and aggravating hypoglycemia- a symptom characterized by high blood sugar.

The endings of peripheral motor nerves secrete a calcitonin-like peptide. It contributes to the suppression of insulin secretion by activating ATP-dependent potassium channels (K+) in the membranes of β-cells, as well as the suppression of glucose uptake by skeletal muscles.

An excess level of leptin, the main regulator of energy metabolism, contributes to the suppression of insulin secretion, leading to insulin resistance of skeletal muscles to adipose tissue.

Thus, insulin resistance includes various metabolic changes: impaired carbohydrate tolerance, obesity, arterial hypertension, dyslipoproteinemia and atherosclerosis. The main role in the pathogenesis of these disorders is played by hyperinsulinemia, as a compensatory consequence of insulin resistance.

Classification and stages of development of type 2 diabetes

Currently, Russian diabetologists classify DM according to the degree of severity, as well as the state of carbohydrate metabolism. However, the International Diabetes Federation (IDF) quite often makes changes in the goals of diabetes care and the classification of its complications. For this reason, Russian diabetologists are forced to constantly change the classifications of type II diabetes accepted in Russia according to the severity and degree of decompensation of the disease.

There are three degrees of severity of the disease:

• I degree - there are symptoms of complications, dysfunction of some internal organs and systems. Improving the condition is achieved by following a diet, prescribing drugs and injections.
• II degree - complications of the organ of vision appear quite quickly, there is an active release of glucose in the urine, problems with the limbs appear. Drug therapy and diets do not give effective results.
• III degree - glucose and protein are excreted in the urine, develops kidney failure. To this extent, the pathology is not treatable.

According to the state of carbohydrate metabolism, the following stages of type II diabetes are distinguished:

• compensated - a normal blood sugar level achieved with the help of treatment, and the absence of sugar in the urine;
• subcompensated - the level of glucose in the blood (up to 13.9 mmol / l) and in the urine (up to 50 g / l) is moderate, while there is no acetone in the urine;
• decompensated - all indicators characteristic of subcompensation are significantly increased, acetone is detected in the urine.

Complications of type 2 diabetes

Acute complications of type II diabetes include:

• Ketoacidotic coma is a dangerous condition in which total intoxication of the body with ketone bodies occurs, as well as metabolic acidosis (increased acidity), acute liver, kidney and cardiovascular failure.
• Hypoglycemic coma is a state of depression of consciousness that develops when sharp decrease the blood glucose level is below the critical level.
• Hyperosmolar coma - this complication develops within a few days, as a result of which metabolism is disturbed, cells are dehydrated, and the level of glucose in the blood increases sharply.

Late complications of type II diabetes are:

• diabetic nephropathy (kidney pathology);
• retinopathy (damage to the retina that can lead to blindness);

• polyneuropathy (damage to the peripheral nerves, in which the limbs lose sensitivity);
• diabetic foot syndrome lower limbs open ulcers, purulent abscesses, necrotic (dying) tissues).

Diagnosis of type 2 diabetes

In order to diagnose type II diabetes, it is necessary to assess the symptoms of the disease and conduct the following studies:

• Plasma glucose determination. Blood is taken from a finger, on an empty stomach. A positive diagnosis of type II diabetes is established in the presence of glucose above 7.0 mmol / l when the analysis is carried out two or more times a day. different days. Indicators may vary depending on physical activity and food intake.
• Glycated hemoglobin (HbAc1) test. Unlike blood sugar readings, HbAc1 changes slowly, so this analysis is a reliable method of diagnosis, as well as subsequent control of the disease. An indicator above 6.5% indicates the presence of type II diabetes.
• Urinalysis for glucose and acetone. In patients with type II diabetes, daily urine contains glucose, it is determined only if the level of glucose in the blood is elevated (from 10 mmol / l). The presence of three or four “pluses” of acetone in urine also indicates the presence of type II diabetes, while this substance is not found in the urine of a healthy person.
• Blood test for glucose tolerance. It involves determining the concentration of glucose two hours after taking on an empty stomach a glass of water with glucose dissolved in it (75 g). The diagnosis of type II diabetes is confirmed if the initial glucose level (7 mmol / l or more) after drinking the solution increased to at least 11 mmol / l.

Type 2 Diabetes Treatment

Treatment of type II diabetes involves the solution of the main tasks:

• compensate for the lack of insulin;
• correct hormonal and metabolic disorders;
• treatment and prevention of complications.

To solve them, the following methods of treatment are used:

1. diet therapy;
2. physical exercise;
3. the use of hypoglycemic drugs;
4. insulin therapy;
5. surgical intervention.

diet therapy

A diet for type II diabetes, like a regular diet, involves the optimal ratio of the main substances contained in the products: proteins should make up 16% of the daily diet, fats - 24%, and carbohydrates - 60%. The difference in the type II diabetes diet lies in the nature of the carbohydrates consumed: refined sugars are replaced by slowly digestible carbohydrates. Since this disease occurs in overweight people, weight loss is the most important condition that normalizes blood glucose levels. In this regard, a caloric diet is recommended in which the patient will lose 500 g of body weight weekly until the ideal weight is reached. However, the weekly weight loss should not exceed 2 kg, otherwise it will lead to excessive loss of muscle rather than adipose tissue. The number of calories needed for the daily diet of patients with type II diabetes is calculated as follows: women need to multiply the ideal weight by 20 kcal, and men by 25 kcal.

When following a diet, it is necessary to take vitamins, since during diet therapy there is an excess excretion of them in the urine. The lack of vitamins in the body can be compensated with the help of rational use useful products, such as fresh herbs, vegetables, fruits and berries. In winter and spring, it is possible to take vitamins in yeast form.

A correctly selected system of physical exercises, taking into account the course of the disease, age and present complications, contributes to a significant improvement in the condition of the patient with diabetes. This method of treatment is good because the need for the use of insulitis is practically eliminated, since during physical exertion glucose and lipids are burned without his participation.

Treatment with hypoglycemic drugs

To date, derivatives of hypoglycemic drugs are used:

• sulfonylurea ( tolbutamide, glibenclamide);
• biguanides, which reduce gluconeogenesis in the liver and increase the sensitivity of muscles and liver to insulin ( metformin);
• thiazolidinediones (glitazones), similar in properties to biguanides ( pioglitazone, rosiglitazone);
• alpha-glucosidase inhibitors that reduce the rate of glucose absorption into gastrointestinal tract (acarbose);
• agonists of glucagon-like peptide-1 receptors, stimulating the synthesis and secretion of insulin, reducing glucose production by the liver, appetite and body weight, slowing down the evacuation of the food bolus from the stomach ( exenatide, liraglutide);
• inhibitors of depeptidyl-peptidase-4, which also stimulate the synthesis and secretion of insulin, reduce the production of glucose by the liver, do not affect the rate of evacuation of food from the stomach and have a neutral effect on body weight ( sitagliptin, vildagliptin);
• inhibitors of sodium-glucose cotransporter type 2 (gliflozins), which reduce the reabsorption (absorption) of glucose in the kidneys, as well as body weight ( dapagliflozin,empagliflozin).

insulin therapy

Depending on the severity of the disease and the complications that arise, the doctor prescribes insulin. This method of treatment is indicated in approximately 15-20% of cases. Indications for the use of insulin therapy are:

• rapid weight loss for no apparent reason;
• the occurrence of complications;
• insufficient effectiveness of other hypoglycemic drugs.

Surgery

Despite the many hypoglycemic drugs, the question of their use remains unresolved. correct dosage, as well as the adherence of patients to the chosen method of therapy. This, in turn, creates difficulties in achieving long-term remission of type II diabetes. Therefore, surgical therapy of this disease - bariatric or metabolic surgery - is gaining more and more popularity in the world. The MFD considers this method of treatment for patients with type II diabetes to be effective. Currently, more than 500,000 bariatric surgeries are performed worldwide every year. There are several types of metabolic surgery, the most common being gastric bypass and mini gastric bypass.

During the bypass, the stomach is cut below the esophagus so that its volume is reduced to 30 ml. The remaining large part of the stomach is not removed, but is choked, preventing food from entering it. As a result of the intersection, a small stomach is formed, to which the small intestine is then sewn, retreating 1 m from its end. Thus, the food will directly enter the large intestine, while processing it with digestive juices will decrease. This, in turn, provokes irritation of the L-cells of the ileum, which contributes to a decrease in appetite and an increase in the growth of cells that synthesize insulin.

The main difference between mini gastric bypass and classical gastric bypass is the reduction in the number of anastomoses (connections of intestinal segments). When performing a traditional operation, two anastomoses are superimposed: the connection of the stomach and small intestine and the connection of different parts of the small intestine. With minigastric bypass, there is only one anastomosis - between the stomach and the small intestine. Due to the small volume of the newly formed stomach and the rapid flow of food into the small intestine, the patient has a feeling of fullness even after taking small portions of food.

Other types of bariatric surgery include:

• sleeve gastroplasty (otherwise it is called laparoscopic longitudinal resection of the stomach) - cutting off most of the stomach and forming a gastric tube with a volume of 30 ml, which contributes to rapid saturation, and also avoids following a strict diet;

• gastric banding - a reduction in the volume of the stomach with the help of a special ring (bandage) superimposed on the upper part of the stomach (this intervention is reversible).

Contraindications for surgical treatment- the patient has esophagitis (inflammation of the mucous membrane of the esophagus), varicose veins esophageal veins, portal hypertension, liver cirrhosis, peptic ulcer or duodenum, chronic pancreatitis pregnancy, alcoholism, serious illnesses of cardio-vascular system or mental disorders, as well as long-term use of hormonal drugs.

Forecast. Prevention

Unfortunately, there is no cure for type II diabetes. However, there are ways to improve the quality of life of patients with this disease.

Today, there are a large number of “bases” where endocrinologists explain to patients what their lifestyle should be like, how to eat right, what foods should not be consumed, what should be daily physical activity.

A huge number of hypoglycemic drugs have also been created, which are improved every year. In order for them to have a positive effect on the body, medicines must be taken regularly.

Practice shows that compliance with all the recommendations of endocrinologists improves the treatment of type II diabetes.

Bariatric surgery is an operative method that improves the quality of life in type II diabetes, according to the MFD.

Significantly improve the condition of patients with this disease allows gastrointestinal operations (therapy), as a result of which the level of glycohemoglobin and glucose in the blood is normalized, the need for the use of antidiabetic drugs and insulin is lost.

Bariatric surgery can lead to significant and sustained remission as well as improvement in type II diabetes and other metabolic risk factors in obese patients. Surgery within 5 years of diagnosis most often leads to long-term remission.

To prevent the occurrence of type II diabetes, the following preventive measures must be observed:

• Diet- with excess body weight, it is necessary to monitor what is included in the diet: it is very useful to eat vegetables and fruits with a low glucose content, while limiting the use of foods such as bread, flour products, potatoes, fatty, spicy, smoked and sweet dishes.
• Strong physical activity- Exhausting workouts are not necessary. The best option would be daily walking or swimming in the pool. Lungs physical exercise, if done at least five times a week, reduce the risk of developing type II diabetes by 50%.
• Normalization of the psycho-emotional state is an integral method of preventing this disease. It is important to remember that stress can cause metabolic disorders leading to obesity and the development of diabetes. Therefore, it is necessary to strengthen stress resistance.