Type 2 diabetes mellitus treated with modern drugs. Treatment of diabetes mellitus of various types: means and methods. Pancreas transplant

Modern methods of diagnosis and treatment of diabetes mellitus
Modern methods of treating diabetes mellitus

DIABETES

Diabetes(DM) is a chronic polyetiological disease that is characterized by hyperglycemia, catabolism of protein, fat and, regardless of the cause, associated with a lack of insulin (absolute or relative).
In diabetes, the fasting blood glucose level is more than 7.2 mmol/l in a double study.

Epidemiology. The number of patients suffering from type 2 diabetes in the world is progressively increasing: from 135 million patients registered in 1995 to 160 million in 2000.
According to WHO experts, by 2015 the number of patients suffering from type 2 diabetes in the world is projected to increase to 300 million people.
According to the American Diabetes Association, 800,000 new cases of diabetes are diagnosed annually, the vast majority of which are patients with type 2 diabetes.

Classification:
1. Clinical classes of diabetes:
1) diabetes mellitus: (fasting blood glucose level more than 7.2 mmol/l) primary (types I and II), secondary;
2) impaired glucose tolerance: obese, normal weight;
3) diabetes in pregnant women.

2. Reliable risk classes: diabetic heredity, obesity, persons who have had impaired glucose tolerance in the past, women who had glucose in their urine during pregnancy, etc.

PRIMARY DIABETES MELLITUS
1. Insulin-dependent diabetes mellitus (IDDM or type I diabetes) is an absolute deficiency of insulin.
A disease that occurs with absolute insulin deficiency, arising as a result of immunopathological processes developing against the background of a genetic, constitutional predisposition.
IDDM is characterized by the onset of the disease in childhood and adolescence, the severity of clinical symptoms, lability of the course, a tendency to ketoacidosis, and the frequent development of microangiopathies.
Insulin replacement therapy in the vast majority of cases is the only way to save the patient’s life.

According to ICD 10 - E10 (insulin-dependent diabetes mellitus).

Etiology and pathogenesis. IDDM is an autoimmune disease. Its development is based on a hereditary defect in chromosome 6-1 associated with the HLA system D3, D4. A certain role is assigned to mumps, measles, Coxsackie viruses, severe stressful situations, and chemicals. Many viruses have an affinity for pancreatic b-cells. The normal immune system resists viruses. With a genetic defect, an immune reaction develops and infiltration of pancreatic islets with lymphocytes occurs.
B lymphocytes produce cytotoxic AT.
b-cells die, and insufficiency in the production of INSULIN develops - diabetes develops.

2. Non-insulin-dependent diabetes mellitus (NIDDM or type II diabetes).
Occurs with relative insulin deficiency.
In the blood of patients, insulin levels are normal or elevated.
The main criteria for NIDDM are: mature and elderly age of patients, often increased body weight, usually a gradual onset of the disease, stable course, absence of ketoacidosis, frequent combination with atherosclerotic lesions of large vessels.

Etiology and pathogenesis. At present, the genetic basis of NIDDM is beyond doubt. Genetic determinants in NIDDM are even more important than in type 1 diabetes.
The genetic basis of NIDDM is confirmed by the fact that in identical twins, NIDDM almost always develops in both (95-100%).
It must be admitted that the genetic defect itself that determines the development of NIDDM has not been fully deciphered.

From today's perspective, two options are being considered.
First: two independent genes are involved in the pathogenesis of NIDDM, one is responsible for impaired insulin secretion, the second causes the development of insulin resistance.
The possibility of a general defect in the glucose recognition system by b-cells or peripheral tissues is also being considered, resulting in either a decrease in glucose transport or a decrease in the glucose-stimulated response of b-cells.
The main pathogenetic factor causing the development of NIDDM is relative insulin deficiency due to tissue insulin resistance.

Insulin resistance (IR) is an impaired metabolic response to exogenous or endogenous insulin (resistance to insulin-dependent glucose uptake).
IR leads to an increase in the level of insulin in the blood plasma compared to that required for the existing glucose level. The concept of IR is applicable to other biological effects of insulin, including its effects on lipid and protein metabolism, vascular endothelial function, and gene expression.

Most patients with this type of diabetes do not require insulin replacement therapy and require dietary treatment or the use of antidiabetic tablets.

According to ICD 10 - E11 (non-insulin-dependent diabetes mellitus).
NIDDM is based on a genetic defect in the b-cells themselves and peripheral tissues, which manifests itself without the influence of external factors.
Insulin sensitivity (insulin resistance) of muscle, fat and liver tissue decreases.
Long-term insulin resistance is compensated by excess production of insulin by pancreatic b-cells (hyperinsulinemia), thereby maintaining a normal level of carbohydrate metabolism.

Hyperinsulinemia is equated to markers of insulin resistance and is considered a precursor to the development of type II diabetes.

Clinical manifestations of diabetes. The most characteristic symptoms of overt diabetes are thirst, polyuria, weight loss, and weakness.
Type I diabetes usually manifests itself acutely, characterized by rapid progression of symptoms and a tendency to develop ketoacidosis. Delay in insulin therapy can be fatal. Diabetes develops especially severely against the background of an associated infection.

Type II diabetes is characterized by a gradual onset, slow progression, and moderate severity of specific symptoms of the disease (thirst, polyuria, etc.). Skin itching, furunculosis, periodontal disease, and complicated obstetric history are common.
As the disease progresses, the specificity of DM symptoms will increase.
It is possible to improve and even completely normalize the condition under the influence of external factors (dietary restrictions, physical activity, etc.).
With a long course of type I and II diabetes, gradually all organs and systems become involved in the pathological process.

Characteristic is the early development and rapid progression of atherosclerosis, leading to MI, cerebrovascular accidents, and encephalopathy. The body's resistance to infections decreases.

Tuberculosis and UTIs often develop. In the absence of proper treatment for diabetes, children develop a pathological symptom complex, including delayed physical and sexual development, hepatomegaly (Mauriac syndrome).

Developed complications of diabetes, the main ones of which are microangiopathy and neuropathy, significantly affect the clinical picture of the disease.
Of greatest importance is damage to the vessels of the fundus, kidneys, and lower extremities.
Diabetic angiopathy is characterized by changes in the caliber of blood vessels, tortuosity of veins, and the presence of microaneurysms; with simple diabetic retinopathy, in addition to the changes described above, pinpoint hemorrhages, exudates, and foci of degeneration appear, which sharply impair vision.

Proliferating retinopathy is characterized by new formation of capillaries, proliferation of fibrous tissue, and hemorrhages into the vitreous, leading to progressive loss of vision resulting in blindness.

Diabetic intercapillary glomerulosclerosis is a late complication of diabetes, which is the most common cause of death in young patients. The basis of kidney damage is thickening of the basement membrane of the glomerular capillaries, deposition of a hyaline-like substance with gradual obliteration of the glomeruli.
Clinical symptoms appear quite late; even moderate proteinuria indicates an advanced pathological process. The first, prenephrotic, stage of glomerulosclerosis is characterized by only moderate proteinuria of a persistent or transient nature. The second, nephrotic, stage is characterized by the development of full-blown NS.
The third stage, nephrosclerotic, is characterized by progressive renal failure and a decreased need for insulin.

When UTI is associated with diabetic glomerulosclerosis, kidney failure can develop very quickly.
A special transient form of pyelonephritis in diabetes is characterized by necrotizing papillitis, septic course, and rapid development of uremia.

Gangrene of the lower extremities in diabetes is the result of many pathological processes: atherosclerosis, microangiopathy, neuropathy.
Diabetic gangrene develops either dry or wet.
Dry gangrene can result in mummification, the formation of a demarcation line and self-sequestration of the affected area.
In these cases, a very limited amount of surgical intervention can be used.
In case of infection or development of wet gangrene, a high amputation is usually required.
One of the variants of trophic disorders is the so-called “diabetic foot”, characterized by damage to one or more joints of the foot, the development of osteolysis of the metatarsal bones (usually IV and V), periarticular infiltration of soft tissues, and the formation of trophic ulcers of the foot.

Pathological changes in the nervous system are characterized by encephalopathy and memory impairment, neuroticism, tearfulness, depression, and sleep disturbances.

Damage to peripheral nerves (diabetic neuropathy) can manifest as radiculopathy, mononeuropathy, polyneuropathy, and autonomic neuropathy.
The most common form is distal polyneuropathy, which is manifested by pain, peresthesia, sometimes cramps, a feeling of weakness, chilliness, and heaviness in the legs. Objectively, sensitivity disorders, decreased reflexes, fibrillary twitching, muscle atrophy, trophic disorders (thinning, dry skin, local hyperkeratosis, atrophic pigment spots, trophic lesions of the nails) are determined.

As the disease progresses, there is a steady decrease in sensitivity, which reduces the severity of the pain syndrome, despite the increase in objective symptoms, and explains the frequency of painless forms of MI, gangrene and arthropathy in diabetes.

Autonomic neuropathy can cause various disorders - impotence, enteropathy, dysuric disorders, hyperhidrosis, etc. Diabetic nephropathy.

The increase in life expectancy of patients with diabetes affected the structure of their mortality. If in the pre-insulin era the mortality rate of patients with type 1 diabetes from ketoacidotic coma was 90%, and life expectancy did not exceed 2-3 years, then after the introduction of insulin therapy in 1922, the situation changed dramatically.

Late vascular complications of diabetes - microangiopathy (diabetic nephropathy) and macroangiopathy (cardiovascular complications) - took first place in the structure of mortality of patients with diabetes.

In the pathogenesis of DN, a significant place is given to the role of transforming growth factor b1 (TGF b1) in DN. This growth factor may be an indicator of glomerular damage in patients with type 2 diabetes.
Hyperglycemia and Apo-E2 lipoproteins in patients with diabetes stimulate the activity of protein kinase C and TGF b1, which contributes to the development of glomerulosclerosis in patients with diabetes 2.

Other factors of kidney tissue damage in diabetes may be: activation of the expression of intracellular adhesion molecules ICAM-1; high activity of lysosomal enzymes, influence of atrial natriuretic factor.
Genes associated with the development of DN were discovered: 5-allele of the microsatellite marker of the angiotensinogen gene, polymorphic gene of endothelial NO synthase (Glu298Asp), CCR5 promoter of the chemokine receptor gene, H63D mutation of the hemochromatosis gene.

The earliest and most reliable manifestation of DN is microalbuminuria.
The term “microalbuminuria” refers to the excretion of albumin in urine in low quantities (from 30 to 300 mg/day).
This amount of protein is not determined by traditional routine urine testing, and therefore the earliest stage of DN may not be diagnosed.
But this stage is the only one reversible with timely administration of pathogenetic therapy.
Subsequently, the amount of protein lost in the urine increases (stage of proteinuria with preserved filtration function of the kidneys) and then renal failure forms.

The inevitability of DN in patients with type 1 and type 2 diabetes requires early detection of microalbuminuria.
Screening for microalbuminuria should be carried out in patients with type 1 diabetes, once a year after 5 years from the onset of diabetes, once a year from the moment of diagnosis of diabetes.
Laboratory examination may reveal hypercholesterolemia, hyponatremia, and hypokalemia.
Proteinuria and hyperazotemia indicate the presence of diabetic glomerulosclerosis, chronic renal failure.
The presence of acetone in the urine, an increase in the concentration of ketone bodies in the blood, and a decrease in blood pH indicate profound metabolic disorders that threaten the development of diabetic coma and require urgent measures.

Diagnostics. Risk factors for diabetes: obesity, heredity, identical twins (if one has diabetes, the other needs to be examined), women who have given birth to large children.

Laboratory diagnostics (normal blood glucose concentration is less than 6.1 mmol/l.
The maximum limit during the day is 8.9 mmol/l.
Required volume of laboratory tests: fasting blood glucose - twice (a diagnostically significant increase in sugar level of more than 130 mg% or 7.2 mmol/l).

Glucose in the blood after eating (a diagnostically significant increase in sugar levels of more than 200 mg% (or 11.2 mmol/l).

Glucose tolerance test (TTGl).
Indications for TSH testing: blood glucose level less than 130 mg% in the presence of risk factors for diabetes and concomitant diseases.
Test conditions: the patient should not reduce the amount of food consumed for 3 days before the test; the patient should fast for 10-16 hours immediately before the test; the test must be performed in the morning.
The sugar level in a blood sample taken on an empty stomach is determined.
After this, within 5 minutes the patient must drink 75 g of glucose dissolved in 250 ml of water.
After 2 hours, the blood sugar level is determined for the second time.
In healthy people, fasting blood sugar (capillary blood) is less than 5.55 mmol/l, after 2 hours it is less than 7.8 mmol/l.
If glucose tolerance is impaired, fasting glucose is less than 6.7 mmol/l, after 2 hours it is more than 11.1.
In the presence of diabetes, fasting glycemia is more than 6.7 mmol/l, after 2 hours - more than 11.1 mmol/l.

The glucose content in the daily urine sample is also determined. Glycemia is examined on an empty stomach and every hour for 2 hours after a single oral glucose load at a dose of 1 g/kg body weight.

Glycated hemoglobin. Hemoglobin is a protein found in red blood cells. Hemoglobin carries oxygen from the lungs to all cells of the body.
Like other proteins, hemoglobin can combine with sugars such as glucose. When this happens, glycated hemoglobin (GGb) is formed.
In other words, GGb is formed as a result of the slow non-enzymatic addition of glucose to hemoglobin A contained in red blood cells. GGB is also present in the blood of healthy people.
GGb reflects hyperglycemia that occurred during the life of erythrocytes (up to 120 days).
Red blood cells circulating in the blood have different ages.
Usually they focus on the average period - 60 days.
The GGb level is an indicator of compensation of carbohydrate metabolism during this period.
Normalization of GGB levels in the blood occurs 4-6 weeks after reaching normal glucose levels.
In patients with diabetes, the level of this compound can be increased by 2-3 times. This test is considered optimal and necessary for controlling diabetes.
Patients with diabetes are recommended to test their GGb levels at least once a quarter.

Differential diagnosis.
1. Diabetes insipidus (characterized by thirst and polyuria, specific gravity of urine less than 1.005).
2. Renal glycosuria (associated with a decrease in the threshold for glucose, moderate and variable).
3. Glucosuria in pregnant women (glucose in the urine with normal levels in the blood).
4. Pregnant diabetes (the placenta produces a lot of anti-insulin hormones).

ACUTE COMPLICATIONS OF DIABETES

Diabetic ketoacidosis (DKA)- clinical-biochemical syndrome with high levels of glucose in the blood, glycosuria, hyperketonemia, DKA - an acute, very serious condition from which the patient cannot recover on his own, death occurs within 3-4 days.
The mortality rate from DKA is 5-6%.
Against the background of increasing hyperglycemia, thirst and polyuria become painful, pronounced protein catabolism and electrolyte losses give rise to severe muscle weakness; the accumulation of incompletely oxidized metabolic products (acetoacetic and b-hydroxybutyric acids) causes acidosis and intoxication phenomena - anorexia, nausea, vomiting, which, in turn, aggravates dehydration and electrolyte losses.
Some patients may experience abdominal pain simulating acute surgical illnesses against this background.
Characterized by the presence of deep, noisy breathing of the Kussmaul type, the smell of acetone in the exhaled air.
Against the background of severe dehydration, shock syndrome develops with cellular hypoxia and impaired microcirculation.
The result of complex metabolic disorders is a disorder of the functions of vital organs - hemodynamic failure, development of acute renal failure, etc.
It should be noted that there may not be a complete loss of consciousness even if the patient’s condition is very serious.
The pathological process is progressive; in the absence of pathogenetic treatment, metabolic disorganization reaches an extreme degree and leads to the death of the patient.

Laboratory data: hyperglycemia more than 300 mg% (18 mmol/l), glycosuria, severe aceturia ++++, acidosis (mild acidosis - pH 7.3 7.2; severe acidosis - 7.2-7.0; severe acidosis - 7.0 or less, pH = 6.8 - incompatible with life).
In peripheral blood: hyperleukocytosis (13-35)x10*9/l with a shift to the left; increase in creatinine (0.2-0.5).

Hyperosmolar coma. A more severe condition than DKA is much less common - 0.001%.
In hyperosmolar diabetic coma, disruption of the central nervous system is manifested by encephalopathy, turning into coma. Violations of CVS function are clinically manifested by tachycardia, decreased blood pressure up to the development of collapse, and anuria. Thromboembolic complications are common. Features of hyperosmolar coma are the absence of ketoacidosis, moderate severity of electrolyte disorders with severe glycemia and associated dehydration.

Laboratory data: hyperglycemia (above 50 mmol/l), increased hematocrit number, leukocytosis is less pronounced, blood pH is normal (7.35), increased creatinine (protein catabolism is in progress); there is no acetone in the urine or only one K Hyperlactic acidemic coma, lactic acidosis is a type of metabolic disorder that occurs in pathological conditions accompanied by hypoxia (CH, respiratory failure, physical overload, etc.), activating the anaerobic pathway of glucose conversion, with the formation of lactic acid.

In patients with diabetes, lactic acidosis develops when treating with biguanides persons who have contraindications to the use of drugs in this group (hypoxia of any origin, alcoholism, infections, etc.).

In the clinical picture of hyperlactic acidemic coma, the phenomena of acidosis and intoxication occur.
A drop in blood pH below 7.2 may be accompanied by hemodynamic disturbances due to a decrease in the sensitivity of the receptor apparatus of the myocardium and blood vessels to the vasopressor effect of catecholamines.

Laboratory tests reveal hyperglycemia (often moderate), decreased blood pH, and increased lactic acid concentration. A hypoglycemic state and coma occur with an overdose of drugs (insulin or sulfonamide drugs) and (or) a violation of the diet.

Renal and liver failure, muscle work, and alcohol consumption predispose to the development of hypoglycemia.
Hypokalemia usually develops suddenly.

The patient feels anxiety, hunger, tremors, sweating, headache, and weakness.
If help is not provided in a timely manner, the condition progressively worsens; agitation, inappropriate behavior, convulsions, and loss of consciousness often occur.
Blood pressure is elevated, tachycardia and profuse sweat are noted.

Diabetes treatment.
Treatment objectives:
1. Achieve adequate control of diabetes (fasting blood glucose level - less than 6.5 mmol/l, after meals - less than 7-8 mmol/l).
2. Normalization of the blood lipid spectrum (to prevent chronic complications).
3. Treatment of complications.
4. When treating pediatric patients, ensure their normal growth and development. Diet is an integral part of all types of diabetes treatment, including in combination with oral hypoglycemic drugs and insulin therapy.
In some cases, in patients with type II diabetes, the diet can be used as an independent method of treatment.
This applies to older people with excess body weight, satisfactory general condition, moderate hyperglycemia, and lack of ketosis.

For NIDDM, a diet is prescribed aimed at normalizing the patient’s body weight.
Since most patients with type 2 diabetes are obese, the diet should generally be low in energy.
Along with a low-energy diet, fasting days (milk, kefir, cottage cheese, etc.) can be used.
This is the main difference from the diet recommended for type I diabetes.
The diet should contain a sufficient amount of vegetables, fruits, herbs - the main sources of vitamins and microelements.

The ratio of the main ingredients in the diet of a patient with diabetes does not differ from that of a healthy person - 60% of the total energy value should be covered by carbohydrates, 24% by fats (mainly vegetable), 16% by proteins.

In cases of severe obesity, the limitation of energy value is achieved by excluding high-energy foods containing carbohydrates - porridge, potatoes.
The daily energy value of food is determined individually for each patient, depending on the ideal body weight (height in cm - 100) and the physical activity performed.
An indicator of the adequacy of a diet for a patient with type II diabetes in combination with obesity is weight loss.

For type 1 diabetes, insulin therapy is prescribed in combination with a physiological diet and diet that provides carbohydrate intake every 3-3.5 hours.
The total energy value of the food ration should completely cover the body's energy expenditure.
The need to exclude easily digestible carbohydrates (sugar and sugary substances) and limit the consumption of foods containing significant amounts of cholesterol (fatty meats, lard, egg yolk, etc.) are acceptable for all patients with diabetes.

Type II diabetes. Here are the “New recommendations from the American Diabetes Association and the European Association for the Study of Diabetes on the control of hyperglycemia in type 2 diabetes” (Diabetes Care 2006;29:1963-72). Dr. David M. Nathan and colleagues (Massachusetts General Hospital, Harvard Medical School, Boston) recall that glycemic control significantly reduces the incidence of diabetes-specific complications in both type 1 and type 2 diabetes mellitus.
The need to start or adjust therapy, according to the new recommendations, is indicated by a HbA1 level of 7% or higher.

The choice of antihyperglycemic drugs is determined by their hypoglycemic effect, extraglycemic effect, safety, tolerability and cost, as well as their effect on other cardiovascular risk factors (hypertension, dyslipidemia).

Currently, there is no convincing data on the benefits of one or another drug or their combination.

The recommended algorithm includes the following steps:
Stage 1 (initial) - changing lifestyle, losing weight, increasing physical activity.
This intervention is low-cost and clinically effective, but effectiveness tends to decline over the first year.

Taking metformin (does not affect weight; low price; gastrointestinal side effects; low incidence of lactic acidosis).

Stage 2 (additional therapy) - insulin (no dosage limit; low price; improvement of lipid profile; need for injections, monitoring; risk of hypoglycemia, weight gain).

Long-acting sulfonylureas (chlorpropamide, glybutride, glipizide SR) are more likely to cause hypoglycemia than glipizide, glimepiride and gliclazide.

Thiazolidinediones (improved lipid profile; high price; risk of fluid retention and weight gain).

Other drugs.
Alpha-glucosidase inhibitors (no effect on weight; common gastrointestinal side effects; taken three times a day; high price).

Exenatide (weight loss; need for injections; frequent gastrointestinal side effects; high price; insufficient data on use in clinical practice).

Glinides (short duration of action; high price; taken 3 times a day).

Conclusion: achieving and maintaining normoglycemia; initial intervention - lifestyle changes, metformin; rapid addition of drug therapy; its correction when target glycemic levels are not achieved; early addition of insulin when target glycemic levels are not achieved.

Next we move on to the details.
Main medications: sulfonylureas and biguanides.
The mechanism of action of sulfonylurea drugs is stimulation of the synthesis of endogenous insulin by b-cells, reducing tissue insulin resistance.

Second generation drugs: glibenclamide (Daonil, Euglucon), gliclazide (Diabeton, Diamicron, Predian), glipizide (Minidiab) and gliquidone (Glyurenorm, Biglinor).
The advantage of the latter is that the drugs are excreted not by the kidneys, but by the gastrointestinal tract, which makes it possible to use them for concomitant kidney damage.

Gliclazide derivatives have an antiplatelet effect, which is very important for patients with NIDDM with an increased risk of vascular lesions.

In recent years, new highly effective drugs with unique properties have been created.
One of them is Diabeton MB (gliclazide).
The new pharmacological form of gliclazide provides gradual release of the drug substance throughout the day with a single dose of 30 mg (1 tablet) before breakfast.

A new dosage form of glipizide is glucotrol XL.
The drug gives a prolonged effect, acting for 24 hours.
III generation sulfonamide - amaryl.
Micronized forms of sulfonamides: maninil 3.5; maninil 1.75; Maninil.
Thanks to the application of a finely porous micronized film to the active substance of the drug, maninil dissolves much faster, is absorbed more efficiently and is delivered to the body tissues. As a result, it exerts its effect much faster - maximum between 1.5-2.5 hours after administration, i.e., at the time of the maximum increase in blood sugar levels after a meal, provided it is taken 30 minutes before meals.
At the same time, the increase in the concentration of the drug in the blood occurs smoothly, which, naturally, does not contribute to a sharp release of insulin while taking micronized forms of maninil, and therefore eliminates the risk of developing hypoglycemic conditions.
A small dose does not mean less effectiveness; on the contrary, when switching to micronized forms of maninil, it is possible to reduce the total daily dose of the drug by 30-40%.
The mechanism of action of biguanides: they reduce the blood glucose level due to a decrease in tissue insulin resistance and a decrease in the absorption of carbohydrates in the intestine, and improve lipid metabolism. Commonly used are buformin (adebit, glybutide, sibin) and metformin (glucophage, diformin).

The most commonly used drug is metformin (Siofor), which lowers blood sugar by accelerating the transport of glucose in the cell and inhibiting the formation of glucose in the liver.
This group of drugs does not cause hypoglycemia.
The most commonly used dose of Siofor is 500 (850) mg 2 times a day.

New classes of antidiabetic tablet drugs: inhibitors of a-glucosidase of the brush border of the intestinal epithelium (acarbose) and benzoic acid derivatives (repaglipid).
Acarbose slows down the breakdown of polysaccharides in the small intestine and thus reduces postprandial hyperglycemia.
Repaglipid is a short-acting drug that very effectively prevents an increase in blood glucose after a meal.

Currently, drugs have appeared in clinical practice, grouped according to their mechanism of action into the group of insulin sensitizers (thiazolidinediones).
By eliminating insulin resistance, they enhance the physiological effect of their own endogenous insulin and at the same time reduce its concentration in the blood.
Valuable properties of the drug are the activation of the catabolism of inflammatory mediators, a decrease in the thickness of the inner wall of arteries due to the elimination of inflammatory and proliferative processes, a decrease in the level of fibrinogen in the blood plasma, as well as atherogenic LDL, while the content of antiatherogenic (HDL) increases.
The whole complex of changes that occur as a result of the action of pioglitazone leads to a slowdown in the progression of atherosclerosis. The drug is taken 1 time per day.

Rosiglitazone, another thiazolidinedione drug, reduces blood glucose by increasing the insulin sensitivity of adipose tissue, skeletal muscle and liver tissue, and improves metabolic control by reducing blood glucose, circulating insulin and free fatty acids.
Combination therapy with rosiglitazone, sulfonylureas and metformin results in a synergistic effect and improves blood glucose control in type II diabetes mellitus.
Taken once orally in doses of 4 mg or 8 mg.

Indications for insulin therapy in NIDDM: decreased production of endogenous insulin by b-cells as a result of long-term metabolic disorders or amylin deposition in the islets of Langerhans.
The following algorithm for resolving the issue of prescribing insulin is recommended.
If there is no effect from various combinations of tableted antidiabetic drugs, insulin is prescribed in addition to them (preferably simple in 4-5 injections) at an initial dose of 12-16 IU/day with a gradual increase in dose until satisfactory compensation is achieved.
The course of insulin therapy lasts 3-4 weeks, after which an attempt is made to cancel it with a gradual reduction in the dose.

The use of combination therapy makes it possible to achieve compensation with the minimum required dose of exogenous insulin, which is important for the prevention of obesity and vascular complications.

Insulin therapy- the most difficult type of treatment for patients with diabetes.
The absolute indications for insulin therapy are diabetic ketoacidosis and diabetic coma, IDDM (type 1), NIDDM with associated absolute insulin deficiency (“insulin-requiring” NIDDM), severe trauma, infection, surgery in a patient with diabetes.

When prescribing insulin, it is necessary to strictly determine the patient's diet (see above).
The recommended diet should be maximally adapted to the working conditions of the patient and the dietary pattern in the family.
It is necessary to train the patient in the technique of insulin therapy and monitoring the effectiveness of treatment.
The dose of insulin is selected individually under the control of glycemia, determined at different times of the day, and glucosuria.

Newly diagnosed diabetes is an indication for hospitalization.
The selection of the insulin dose should be carried out in a hospital setting.

Based on the duration of action, insulins are divided into short-, medium- and long-acting drugs.

Insulins also differ in the degree of purification.
Basic information about the insulins used.

Short-acting insulins (so-called simple insulin) are an aqueous solution of insulin with the addition of preservatives and stabilizers and act for 6-8 hours.
Prolongation (medium- and long-acting insulins) of the effect of insulin preparations is achieved by adding sorbents that bind insulin molecules and ensure their gradual release into the blood.
Aminoquinuride, neutral protamine Hagedorn (isophane insulin, NPH insulin), amorphous zinc suspension (CS-A), crystalline zinc suspension (CS-K) and a mixture of 30% amorphous 70% crystalline zinc- suspensions (30/70TSS-A/TSS-K).

In recent years, a significant number of so-called mixed insulins have appeared, which are a mixture of a certain amount of short- and long-acting insulin (most often NPH insulin).
The ratio of regular and long-acting insulin is indicated on the bottle as a fraction. For example: 30/70 is an insulin preparation, 100 units of which contain 30 units of regular insulin and 70 units of long-acting insulin. Mixts are the drugs of choice for the treatment of insulin-requiring type 2 diabetes.

Regimes of insulin administration: single administration when using long-acting drugs, double administration when treating with intermediate-acting insulin.
In certain situations (ketoacidosis, urgent surgery, etc.), short-acting insulin is used.

Combinations of insulins with varying durations of action are often prescribed.
In accordance with the onset and maximum effect of the insulin used, meals are distributed throughout the day.

The most effective method is basic bolus insulin therapy, in which the patient receives one or two injections of long-acting insulin (the so-called “basal dose”), against which 4-8 units of short-acting insulin are administered before each meal, for which Novopen-type syringes are used. -1", "Plivapen-2 and 1" for injections of short-acting human insulin (homoral).
The syringe pen "Novopen-2" is used for injections of long-acting insulin (homofan, protafan).
Very thin needles make injections almost painless.
The method is the most physiological, simulating the function of the insular apparatus.

Ideal compensation of diabetes mellitus with insulin is associated with the risk of developing hypoglycemic conditions.
Therefore, in the case of a labile form of the disease, severe cerebral atherosclerosis, alcohol abuse, and the presence of mental disorders, strict compensation for diabetes is not indicated.

Methodology for selecting an adequate daily dose of the drug.
This process consists of two stages: choosing the minimum initial dose and its subsequent adjustment.
When selecting a dose, only short-acting insulin preparations are used.

There are several empirical methods for choosing the minimum daily dose.
1. 5% of the sugar value of food is subtracted from daily glucosuria and the result is divided by 5.
The resulting daily dose of insulin in units is usually divided into 4 injections: before breakfast, lunch, dinner and at night in a ratio of approximately 3:3:2:1 - 3:2:2:1.
2. Begin insulin administration with a daily dose of 20 units, which is known to be safe for severe decompensation, dividing it into 2 (12 units + 8 units) or 4 (6 units + 6 units + 4 units + 4 units) before meals at equal intervals.
As a rule, the initial dose of insulin does not provide compensation, therefore, it is subsequently adjusted by gradually increasing it daily by 4-6 units, focusing on the indicators of hyperglycemia and glucosuria at different periods of the day.

To a large extent, the success of dose selection depends on compliance with the dietary regimen and the frequency of determining carbohydrate metabolism indicators.
The selection of the daily dose of insulin is considered complete when good compensation of metabolic processes is achieved.
From this moment on, the patient is transferred to constant insulin therapy using long-acting insulin preparations.

Treatment of complications diabetes mellitus
There are no effective means of pathogenetic therapy for vascular complications of diabetes; this makes the most complete compensation of metabolism necessary.
In the presence of manifestations of angiopathy, drugs of various groups are used - angioprotectors, anabolic steroids, drugs that improve the rheological properties of blood, antioxidants, aldoreductase inhibitors, hypolipidemic agents, etc.

For proliferating retinopathy, laser photocoagulation is used. In diabetic nephropathy, it is necessary to eliminate UTIs and hypertension.
Diabetic gangrene requires hospital treatment.
For dry gangrene, local manipulations are not indicated; hyperbaric oxygenation is useful.
The affected area should be open to air.
For inflammatory infiltration in a limited area, radiotherapy is used.
For neuropathy, therapy is supplemented with analgesics, sedatives, and vitamins.
For enteropathy, cholinomimetics and cholinesterase inhibitors are used.

Diabetic coma.
Diabetic diabetes is a condition that requires urgent hospitalization and emergency treatment measures aimed at combating hyperglycemia, dehydration, electrolyte disturbances, acidosis. In the hospital, before treatment, urgent studies are carried out to confirm the diagnosis; blood test (characterized by leukocytosis, high hemoglobin levels, hyperglycemia, hyperazotemia), general urine test, for sugar, acetone.

Therapy is carried out under the control of these indicators; monitoring of ECG, ionogram, pH, osmolarity and blood gases is necessary.

In case of indomitable vomiting, it is advisable to lavage the stomach with a soda solution; Bladder catheterization may be required to control urine output.
Insulin therapy is carried out with simple insulin, which is administered intravenously in an isotonic sodium chloride solution at a rate of 12-16 U/hour.
The rate of insulin administration is further adjusted in accordance with the dynamics of glycemia; when its level decreases to 12-13 mmol/l, insulin administration continues in a 5% glucose solution at a rate of 4-8 U/h.

Insulin administration should not be stopped until the condition is completely normalized and hemodynamics are stabilized.
At this stage, you can switch to fractional subcutaneous injection of insulin in small doses (8-12 units every 6 hours) while taking easily digestible carbohydrates.
After eliminating acetonuria, long-acting insulin is prescribed. Rehydration therapy should begin immediately upon diagnosis.
In the first hour, the patient should receive 1 liter of fluid (Ringer's solution, isotonic sodium chloride solution).
Subsequently, the rate of administration of solutions depends on the patient’s condition, blood pressure level, and diuresis.

For long-term hypovolemia, oncotically active drugs are used - plasma, rheopolyglucin, etc.
The total amount of fluid administered is usually 3.5-6 l/day.
When treating patients with cardiovascular disease, one should be wary of pulmonary edema.
If the level of potassium in the serum is below 4 mmol/l, already at the first stage of treatment, a 1% solution of potassium chloride (in an isotonic sodium chloride solution) is administered. A decrease in glycemia is accompanied by compensation for the deficiency of intracellular fluid and potassium.
In this regard, as glycemia decreases, 5-10 ml of a 10% potassium chloride solution should be added for every 500 ml of solution.
Against the background of complex therapy, the existing acidosis is eliminated without additional administration of sodium bicarbonate.
The use of alkaline solutions is indicated only at pH values ​​less than 7.
If there is a threat of developing cerebral edema, the use of GCS is indicated.
According to indications, vasotonics, SGs, and antibiotics are used.

When a diagnosis of hyperosmolar diabetic coma is made, you should immediately begin to replenish water and electrolyte losses. The rate of rehydration is controlled by the level of blood pressure, central venous pressure, and diuresis.
Control of blood osmolarity is desirable; with very high hyperosmia, it is permissible to administer hypotonic solutions of sodium chloride (0.45%).
However, it should be borne in mind that a rapid decrease in blood osmolarity with persistent hyperosmia in the cerebrospinal fluid may be complicated by cerebral edema.
Insulin therapy should be carried out more carefully than with ketoacidosis due to the danger of sudden changes in blood osmotic pressure.
The initial dose of insulin is 8-12 units/hour.
To prevent thromboembolic complications, the use of anticoagulants is indicated.
Broad-spectrum antibiotics are prescribed to fight the infection.
During the treatment period, measures are taken to eliminate the causes of the coma.

In case of lactic acidosis, sodium bicarbonate is used under the control of CBS to combat acidosis and improve the conditions of peripheral circulation.
In severe cases, the use of Tris buffer, which penetrates cells more quickly, is indicated.
It is advisable to start insulin administration with a 5% glucose solution intravenously; hyperglycemia is usually easily corrected.
To improve capillary blood flow, low molecular weight dextrans are used.

Oxygen therapy is widely used.
The initial symptoms of hypoglycemia are usually easily eliminated by timely intake of carbohydrates.
When a coma develops, a 40% glucose solution (20-100 ml) is injected intravenously until the patient comes out of the coma, after which the patient must take carbohydrates (bread, potatoes, porridge).

In severe cases, restoration of consciousness does not occur due to the development of hypoxia and cerebral edema.
In this case, the administration of diuretics and corticosteroids is indicated.

It is impossible not to note the successes of cellular technologies: Bone marrow stem cells are already transplanted into the diseased pancreas of patients with type 1 diabetes, where they turn into beta cells and produce insulin.
Amazingly, cell technology also helps cells that do not respond to insulin in patients with type 2 diabetes.
Stem cell transplants fuse with the defective cells and give them the genetic material responsible for correcting the problem.

And that's not it. The use of endothelial progenitor cells, bone marrow hematopoietic cells, bone marrow stromal (mesenchymal) cells and adipose tissue can increase the number of peripheral insulin receptors, and therefore increase the sensitivity of body tissues to it.
In addition, the condition of peripheral vessels and blood circulation in them significantly improves, which helps to partially or completely eliminate the problem of vascular complications and related diseases.

Many patients who underwent cell therapy were able to reduce the amount of sugar-lowering medications they consumed, or the amount of insulin they were forced to inject themselves with before, and in some cases even completely abandon maintenance therapy.

The combination of cellular technologies with traditional classical methods of treating diabetes provides a manifold increase in effectiveness in the treatment of this dangerous disease and gives hope for the possibility of a complete cure for diabetes in the future.

SECONDARY SYMPTOMATIC DIABETES MELLITUS
Occurs in pathologies of the endocrine system:
1. Cushing's disease or symptom (disease of chronic excess cortisone). 2. Acromegaly (excess growth hormone).
3. Pheochromocytoma (a tumor that produces catecholamines in excess).
4. Kohn syndrome (primary hyperaldosteronism). Under the influence of aldosterone, potassium levels decrease, and it is necessary for the utilization of glucose.
5. Glucogonoma (tumor of L cells of the islets of Langerhans: patients are exhausted, with ulcers on the extremities).
6. Secondary pancreatic diabetes: after removal of the pancreas, with pancreatic cancer (body and tail).
7. Iron accumulation disease - hemachromatosis (normally, the level of iron in the blood is regulated by a feedback mechanism. With hemachromatosis, more iron is absorbed than necessary, and it enters the liver, pancreas, skin: dark gray skin, enlarged liver, diabetes).
8. Diabetes associated with malnutrition (E12).

In order to achieve maximum results in the treatment of type 2 diabetes, it is necessary to take an integrated approach. It involves taking medications, following a medical diet and regular physical activity. Folk remedies will also come to the rescue.

Pharmaceuticals

Medicines used in the treatment of type 2 diabetes have the following effects:

• Stimulates insulin production. In normal quantities, insulin can no longer cope with the distribution of blood glucose among its main consumers - the liver, muscles, and adipose tissue. Therefore, the pancreas has to increase insulin production. Over time, the cells producing insulin are depleted, and its secretion decreases - the disease enters the stage when it is necessary to administer insulin by injection;
• Reduces the resistance (stability) of body tissues to insulin.
• They inhibit the production of glucose or its absorption from the gastrointestinal tract.
• Correct the ratio of various lipids in the blood.

Drug therapy for type 2 diabetes is not based on the additional administration of insulin, but on taking drugs that increase the sensitivity of peripheral tissues to insulin, and drugs that reduce blood sugar levels by optimizing its lipid profile or blocking the absorption of carbohydrates from food.

In the modern standard treatment regimen for type 2 diabetes, the following groups of drugs are used:

1. Sulfonylurea derivatives . On the one hand, drugs in this group activate insulin production, and on the other hand, they reduce tissue insulin resistance.
2. Metformin – increases the sensitivity of body tissues to insulin, against the background of which the patient’s weight decreases and the lipid composition of the blood improves.
3. Thiazolidinone derivatives – reduce sugar levels and normalize the ratio of lipids in the blood.
4. Alpha-glucosidase inhibitors – block the absorption of carbohydrates in the gastrointestinal tract.
5. Dipeptidyl peptidase-4 inhibitors– increase the sensitivity of pancreatic beta cells to sugar.
6. Incretins – increase sugar-dependent insulin production and reduce excessive glucagon secretion.

At the beginning of treatment, one drug is usually used; if there is no effect, they move on to complex therapy with several drugs, and if the disease progresses, insulin therapy is introduced. With proper treatment of type 2 diabetes, insulin injections can be discontinued over time, maintaining pancreatic function at a normal level.

A low-carbohydrate diet is an important part of treatment

Doctors consider following a low-carbohydrate diet to be more important than taking medications in the treatment of type 2 diabetes. At the initial stages of the disease or at the so-called stage of prediabetes (insulin resistance of body tissues has already been identified, but blood sugar in the morning is still close to normal), the condition can only be normalized through diet.

The diet involves the following rules:

1. Potatoes, if not excluded from the diet, then be minimized. Soak in water before cooking.
2. Monitor the amount of carrots, beets, and legumes in your diet.
3. Without restrictions, you can eat different types of cabbage, pumpkin and leafy green vegetables, bell peppers, and eggplants.
4. Fruits and berries, except bananas, figs, persimmons and grapes, can be eaten 1-2 pieces per day.
5. Among the cereals, you should prefer pearl barley, oatmeal, corn, and buckwheat.
6. Fats are vegetable.
7. Instead of sugar, use sweeteners based on fructose or sorbitol (very moderately), or better yet, sweeteners made from stevia.
8. Salt will have to be limited to a minimum.
9. It is preferable to eat bread made from whole grain flour or with bran (see also - how to choose bread for diabetes).

It is highly undesirable to use:

• Fatty fish (sturgeon, chum salmon, salmon, trout, eel). This also applies to meat (pork, duck, goose, fatty beef).
• Sausages and cheeses with high fat content.
• Rice and semolina.
• Carbonated drinks, packaged juices.
• Baked goods, sweets (even those sold in the diabetic section).

Alcohol and smoking are prohibited. Why? Answer .

There is a numbered medical diet developed for diabetics - number 9. It involves split meals (5-6 times a day), as well as all cooking methods, except frying. The diet is compiled as follows:

• Squirrels – 80-90 g (55% animals).
• Fats – 70-80 g (30% vegetable).
• Carbohydrates – 300-350 g.

Here is an approximate diet menu table No. 9 for the day:

1. For breakfast – 200 g of low-fat cottage cheese with permitted fruits.
2. Snack – 1 orange or grapefruit.
3. Dinner – vegetable soup with a slice of bran bread, boiled beef.
4. Snack – 150 g vegetable salad.
5. Dinner – low-fat steamed fish with a vegetable side dish.
6. 2-3 hours before bedtime - a glass of milk.

Read more about nutrition rules for type 2 diabetes.

Physical activity as a method of combating type 2 diabetes

Daily physical activity is a way to increase glucose consumption and reduce tissue resistance to insulin. The mechanism of this therapeutic method is simple: working muscles need nutrition (glucose) and therefore naturally increase their sensitivity to insulin. The same thing happens in the liver, since muscles that have used up their energy reserves “demand” from the liver the glycogen it has stored, and it needs to replenish the reserve.

Thus, an increase in physical activity, or, to be more precise, the restoration of normal physical activity for a person, also normalizes carbohydrate metabolism in tissues.

For patients with type 2 diabetes, it is very important to introduce walking, swimming, cycling, yoga, gymnastics or other types of feasible physical activity for 30-60 minutes a day into their daily practice.

Folk remedies against type 2 diabetes

Traditional medicine will not completely cure diabetes, but it helps maintain sugar levels within a healthy range:

• Buckwheat grain. Young raw buckwheat is poured with 1 liter of sour milk and left overnight. In the morning you should eat it as breakfast. Can be used every 2nd day or less often.
• Flax seeds. Take 2 tbsp. l. seeds, grind thoroughly and pour in 0.5 liters of boiled water. Put on gas, bring to a boil and hold for 5-7 minutes. Consume in the morning on an empty stomach for 60 days.
• Celandine . Dry herb is added to a half-liter jar until a quarter of the volume is filled. Then it is filled to the brim with boiling water. Let it sit for several hours. 100 ml of decoction is taken daily 15-20 minutes before meals 3 times. When all the infusion has been drunk, you need to take a break of 15 days. Treatment can be carried out 3 times per year.
• White beans . Pour filtered water into a glass and add 15 beans. Leave it overnight and eat it on an empty stomach in the morning. A few doses per week will be enough.

New in the treatment of type 2 diabetes

Since the main cause of peripheral tissue insulin resistance is obesity, it is logical to direct treatment specifically towards reducing fat mass. This can be done not only through general weight loss, but also by using medicinal methods to reduce the number of fat cells, primarily in the liver.

Currently being tested on animals mitochondrial uncoupling method . The drug niclosamide ethanolamine, developed by scientists, helps destroy excess fatty acids and sugar. If the trial is successful, the new method will revolutionize the treatment of type 2 diabetes.

Another promising direction is stem cell treatment . The developers of the method believe that stem cells grown on the basis of the patient’s cellular material, when introduced into the body, will go to the most depleted organs and replace damaged tissues. In the case of diabetes, the composition of the beta cells of the pancreas will be updated and, accordingly, the glucose-dependent secretion of insulin and its uptake by tissues will be normalized.

Another area in which scientists are looking for a solution to the problem of diabetes is the normalization of carbohydrate metabolism due to enriching the patient’s diet with plant fiber . In this case, the new is the well-forgotten old. An unhealthy diet, poor in fresh plant foods, leads to tissue obesity and diabetes. This means that it is necessary to optimize the composition of the diet, even if not through food, but with the help of fiber-containing preparations.

Already today there are enough dietary supplements on the market with plant cellulose that reduce the absorption of carbohydrates, cleanse the gastrointestinal tract, and reduce appetite. And although this cannot be called a full-fledged drug for the treatment of type 2 diabetes, fiber, along with other methods, increases the effectiveness of the fight against the disease.

In addition, every diabetic should know the rules for preventing type 2 diabetes.

Features of treatment in men, women and children

The above treatment methods are suitable for all patients with diabetes, but there are some special features for men, women and children.

Men

Type 2 diabetes in men causes a significant blow to the reproductive system:

• The number of living sperm in the seminal fluid is significantly reduced, which leads to infertility.
• High blood sugar leads to decreased testosterone levels, which affects libido.
• The blood supply to the organs of the reproductive system sharply decreases, which leads to partial or complete impotence.

Therefore, treatment of type 2 diabetes in men also involves a set of therapeutic measures to minimize the above-described consequences of the disease. If the patient follows all the doctor’s recommendations both regarding the treatment of diabetes and the symptomatic treatment of sexual dysfunction, his quality of life in all respects remains at a fairly high level.

Women

The course of type 2 diabetes mellitus in women is significantly influenced by hormonal levels, or rather by its fluctuations associated with the menstrual cycle, pregnancy, and menopause.

Thus, blood sugar increases a few days before menstruation and decreases with its onset. The same picture, only on a larger scale, is observed during pregnancy - sugar increases significantly in the second half of pregnancy and decreases after childbirth. Glucose levels during menopause cannot be clearly predicted - they change unpredictably, just like hormonal levels in general during this period.

Against this background, when treating diabetes in women, special attention is paid to regular self-monitoring of blood glucose, as well as psychological health. For neuroses, herbal infusions are highly recommended.

Children

In children, type 2 diabetes is manifested and treated in the same way as in adults. Particular attention is paid to early diagnosis, without drug treatments for diabetes. Since any medications have side effects and affect a fragile child’s body more negatively than an adult.

Video: Drug-free treatment for type 2 diabetes

Along with standard methods of treating type 2 diabetes, a variety of proprietary methods are widely offered today. One of these methods will be discussed in the following video:

In the next article we will talk in detail about the diagnosis of type 2 diabetes. We will explain the causes of its appearance, symptoms, other treatment methods and prevention for complications.

Treatment of type 2 diabetes mellitus has been the topic of many studies in recent years. Medicine and pharmacology are actively looking for new methods to combat the disease. While they are being developed, today treatment is a comprehensive program that involves proper nutrition, an active lifestyle and, in extreme cases, medication.

For quotation: Ametov A.S. Modern methods of therapy for type 2 diabetes mellitus // RMZh. 2008. No. 4. P. 170

According to experts from the World Health Organization: “Diabetes mellitus is a problem of all ages and all countries.” Currently, diabetes mellitus (DM) ranks third among the direct causes of death after cardiovascular diseases and cancer, therefore, the solution to many issues related to this disease has been raised in many countries of the world at the state and federal level.

According to the International Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (1997), diabetes mellitus is a group of metabolic disorders characterized by hyperglycemia, which results from defects in insulin secretion, insulin action, or a combination of both.

Controltype 2 diabetes mellitus

There is now growing evidence worldwide that effective control of diabetes can minimize or prevent many of its complications.

In relation to the effective management of diabetes, there is compelling evidence suggesting that improving glycemic control can significantly reduce the risk of developing both micro- and macroangiopathy.

An analysis of the 10-year DCCT (Diabetes and Complications Control) study showed that for every percentage reduction in glycated hemoglobin, the risk of developing microvascular complications (retinopathy, nephropathy) decreased by 35%. In addition, the results of this study clearly demonstrated that aggressive glycemic control, along with normalization of blood pressure, significantly reduces the risk of coronary heart disease, cerebrovascular disease and peripheral angiopathy in patients with type 2 diabetes. Based on this, the main goal of treating the disease is to compensate for carbohydrate metabolism disorders as completely as possible. Only the use of complex and pathogenetically based therapy, taking into account the chronic course of the disease, the heterogeneity of metabolic disorders, the progressive decrease in β-cell mass, the age of patients and the danger of hypoglycemia, as well as the need to restore impaired insulin secretion and achieve effective long-term glycemic control will achieve this goal.

Currently, there is no cure for type 2 diabetes, but it can be managed well and you can live a full life.

The type 2 diabetes management program includes the following ways to solve the main problems:

Lifestyle changes (diet therapy, exercise, stress reduction);

Drug treatment (oral hypoglycemic drugs, incretin mimetics, insulin therapy).

Despite numerous published works on the management of type 2 diabetes mellitus, published recently, not all doctors know the algorithm for treating this serious disease. A revised American Diabetes Association (ADA) and European Association for the Study of Diabetes (EASD) Consensus Statement on the management of hyperglycemia in type 2 diabetes has now been developed and published.

Table 1 summarizes various current antidiabetic interventions based on their effectiveness, advantages, and disadvantages.

Goals of therapy

A fundamentally important point is the objective digital criteria for compensation of type 2 diabetes mellitus. In 1999, guidelines for the care of patients with type 2 diabetes were published, which presented criteria for compensation of the disease. It is important to pay special attention to the need for more stringent control of not only carbohydrate metabolism, but also lipid metabolism, as well as blood pressure indicators through the prism of vascular risk, or the risk of developing fatal vascular complications of type 2 diabetes mellitus (Table 2–4).

Choice of therapy and its role in the treatment of type 2 diabetes mellitus

Numerous studies around the world are focused on finding effective treatments for diabetes. However, we should not forget that in addition to drug therapy, recommendations for lifestyle changes are no less important.

Basic principles of diet therapy

Fractional balanced meals 6 times a day, in small portions, at the same time, which helps maintain weight within normal limits and prevents sudden postprandial changes in glycemic levels

If you are overweight, a low-calorie diet (≤1800 kcal) is indicated.

Limiting simple, easily digestible carbohydrates (sugar and products containing sugar, honey, fruit juices)

Increasing consumption of fiber-rich foods (from 20 to 40 g per day)

Limit your intake of saturated fat ‹<10%, полиненасыщенных ‹<10%; предпочтение следует отдавать мононенасыщенным жирам

The daily amount of protein in food should be 1.0–0.8 g/kg body weight; in case of kidney pathology, this amount should be reduced (Fig. 1)

Limiting salt intake to 3 g per day, due to the high risk of developing arterial hypertension and nephropathy. It should be taken into account that the daily amount of unsalted foods already contains 1.5–2.0 g of salt

Limiting alcohol consumption given the high caloric content and risk of hypoglycemia (<30 г в сутки)

The diet should be rich in vitamins and contain the required amount of microelements. In winter and spring, it is recommended to take tableted multivitamins.

Physical activity in treatmenttype 2 diabetes mellitus

The type of physical activity, its intensity, duration and frequency should be individually selected for each patient, taking into account age, initial physical activity, the general condition of the patient, the presence of diabetes complications and concomitant diseases (Fig. 2).

It is important to note that physical activity not only has a positive effect on glycemic indicators, promoting the utilization of glucose (and this effect persists for several hours after the end of physical exercise), but also improves lipid metabolism (reduces the level of triglycerides, which contribute to the development of microangiopathy, and increases the level of high-density lipoproteins, which prevent the development of atherosclerosis), and also have a positive effect on the blood coagulation system (increase fibrinolytic activity and reduce blood viscosity, platelet aggregation and fibrinogen levels).

In addition, physical exercise has a beneficial effect on the cardiovascular system: it increases the efficiency of cardiac output, promotes the electrical stability of the myocardium, reduces oxygen consumption by the heart muscle, reduces and stabilizes blood pressure, and improves blood circulation in the muscles.

It is equally important that physical activity causes positive emotions and helps to resist stressful situations, leads to favorable hormonal changes: they reduce the level of stress hormones, increase the level of “pleasure hormones” (endorphins) and testosterone and, most importantly, lead to a decrease in insulin resistance and hyperinsulinemia.

It should be remembered that physical activity reduces blood sugar if the initial glycemic level is less than 14 mmol/l. When the blood glucose level is above 14 mmol/l, physical exercise is contraindicated, since it does not cause a decrease, but an increase in blood sugar and enhances ketogenesis. Also, physical activity is contraindicated when the glycemic level is below 5.0 mmol/l. Therefore, before, during and after exercise, it is necessary to monitor blood sugar levels, and in the presence of concomitant cardiovascular diseases, also blood pressure (BP) and heart rate (HR).

Medication managementtype 2 diabetes mellitus

The Consensus Statement of the American Diabetes Association and the European Association for the Study of Diabetes emphasized that, in general, a glycated hemoglobin of 7% is the reference point on which decisions are made. However, if we talk not about general, but about individual goals, then in this case glycosylated hemoglobin should be as close as possible to 6%. Thus, the Consensus Statement stated that HbA1c≥7% should be considered as an indication for action to change therapy.

In this regard, it was noted that the positive effect of a lifestyle change program, primarily aimed at reducing weight and increasing physical activity, can be observed quite quickly, even before a significant decrease in body weight is recorded. However, the limited long-term effect of lowering glycemic levels on a long-term basis dictates the need for drug therapy in most patients. It was also emphasized that the choice of treatment goals and the medications to be used to achieve them should be individualized for each patient, balancing the potential reduction in glycated hemoglobin and the long-term beneficial impact on the risk of developing complications with side effects, drug tolerability and cost of treatment.

According to the experts who took part in the development of the Consensus Resolution, due to the fact that lifestyle changes do not allow maintaining metabolic control for a long time, at the first stage metformin should be prescribed simultaneously, almost at the stage of diagnosis. In their opinion, metformin is recommended in the initial stages of pharmacological treatment, in the absence of special contraindications, due to its effect on glycemic levels, absence of weight gain and/or hypoglycemia, usually with a low level of side effects, good tolerability and relatively low cost (scheme 1) .

Biguanides

It should be noted that biguanides began to be used in the treatment of type 2 diabetes more than 50 years ago. However, due to frequent cases of lactic acidosis when taking phenformin and buformin, guanidine derivatives were practically excluded from the treatment of patients with diabetes. It is known that the incidence of this complication varies among different drugs. The only drug approved for use in many countries is metformin.

The hypoglycemic effect of metformin is due to several mechanisms of action not related to insulin secretion by β-cells. Firstly, metformin, in the presence of insulin, suppresses the production of glucose by the liver by increasing the sensitivity of hepatocytes to insulin, reducing gluconeogenesis, activating lactate metabolism, increasing glycogen synthesis and reducing glycogenolysis. Secondly, it reduces insulin resistance at the level of peripheral tissues (fat and muscle) and the liver by enhancing and potentiating the action of insulin, increasing the affinity of receptors for insulin, restoring impaired post-receptor signal transmission links, and increasing the number of insulin receptors in target cells. Thirdly, metformin increases glucose utilization as a result of anaerobic glycolysis. Fourth, metformin somewhat slows down the absorption of glucose in the intestine, which in turn leads to a smoothing of postprandial peaks of glycemia. This may be due to a decrease in the rate of gastric emptying and small intestinal motility. Fifth, when taking metformin, there is an increase in anaerobic utilization of glucose in the intestine. Thus, taking into account the listed main mechanisms of action of this drug, it is more correct to talk not about a truly hypoglycemic (sugar-lowering) effect, but about an antihyperglycemic effect that prevents an increase in blood sugar.

Experimental and clinical studies have shown that metformin has a beneficial effect on the lipid spectrum and the blood coagulation system. It reduces plasma triglyceride concentrations by an average of 10–20%. A significant decrease in the concentration of total cholesterol and LDL cholesterol is likely due to a decrease in their biosynthesis in the intestines and liver. Metformin reduces postprandial chylomicron and chylomicron remnant concentrations and slightly increases HDL cholesterol concentrations.

The drug enhances the processes of fibrinolysis, as a result of which the risk of thrombosis and vascular complications of diabetes is reduced.

In addition, metformin has a weak anorexigenic effect.

The BIGYanides and Prevention of the Risk of Obesity study demonstrated that metformin in 324 patients with abdominal obesity was associated with greater reductions in body weight, plasma insulin, total cholesterol, and fibrinolysis compared with placebo.

In general, the drug is well tolerated by most patients. Among the side effects of metformin, one should note diarrhea and other phenomena from the gastrointestinal tract (metallic taste in the mouth, anorexia, nausea, vomiting), which are observed in almost 20% of patients at the beginning of therapy, and then go away on their own within a few days. Apparently, these disorders are associated with the effect of metformin on slowing the absorption of glucose in the small intestine. Accumulating in the gastrointestinal tract, carbohydrates cause fermentation processes and flatulence, which can create some inconvenience for the patient. Prevention or reduction of the negative effect of the drug on the gastrointestinal tract is ensured by prescribing minimal doses of the drug with gradual titration at intervals of several days.

It was recommended to start metformin therapy with low doses - 500 mg, taken 1 or 2 times a day with meals (breakfast and/or dinner). After 5–7 days, if no side effects from the gastrointestinal tract are noted, the dose of metformin can be increased to 850 mg or 1000 mg after breakfast and after dinner. If side effects develop in response to an increase in dose, the dose is reduced to the original dose, followed by attempts to increase the dose later.

It has been noted that the maximum effective dose of metformin is usually 850 mg twice daily, with moderately higher efficacy when the dose is increased to 3000 mg. However, side effects may limit the use of higher doses (Table 5).

In general, giving due attention to the presented Consensus Resolution, it should be noted that despite the presence of adherents of metformin both in our country and abroad, there is another point of view, indicating the need to take into account that defects in insulin secretion play an important role in the development and progression of type 2 diabetes mellitus, and therefore the role of other drugs for the treatment of type 2 diabetes mellitus must be properly assessed.

Sulfonylureas

The main mechanism of action of sulfonylureas (SUs) is to stimulate insulin secretion. SM drugs affect pancreatic β-cells, in particular, by binding and closing K-ATP-dependent channels of the cell membrane. As a result, depolarization of the cell membrane occurs, opening of Ca2+ channels, influx of Ca2+ and exocytosis of insulin from granules.

It is important to note that ATP-dependent K+ channels are found not only in the pancreas, but also in the myocardium, smooth muscle, neurons and epithelial cells. Therefore, an extremely important characteristic for SM preparations is the specificity of binding to receptors located precisely on the surface of pancreatic β-cells. The extrapancreatic effects of SM drugs have not been convincingly proven; most likely, they are associated with a decrease in glucose toxicity due to insulin stimulation.

Treatment with SM drugs, as a rule, begins with the lowest possible doses, if necessary, gradually increasing once every 5-7 days until the desired level of glycemia is achieved. For patients with severe glucose toxicity, treatment can be started immediately with the maximum dose, then, if necessary, reducing it as the blood glucose level decreases (Table 6).

Side effects of SM drugs include hypoglycemia, weight gain, skin rash, itching, gastrointestinal disorders, blood disorders, hyponatremia, and hepatotoxicity.

Thiazolidinediones (glitazones)

Drugs in this group belong to a new class of oral hypoglycemic agents acting at the level of peroxisome proliferator-activated receptors (PPARs). These receptors are located mainly in the nuclei of fat and muscle tissue cells. PPAR-γ activation improves insulin sensitivity through increased expression of numerous genes encoding proteins responsible for the metabolism of glucose and free fatty acids (FFAs). As a result, insulin sensitivity improves at the level of the liver, muscle and fat tissue.

Thiazolidinediones reduce insulin resistance by increasing the number of glucose transporters (GLUT-1, GLUT-4) and improving the conditions for glucose utilization by tissues, reducing the level of FFA and triglycerides in the blood, enhancing insulin peptide, suppressing glucose production by the liver, reducing tumor necrosis factor and remodeling of adipose tissue .

In Russia, 2 drugs from the glitazone group are registered and approved for clinical use: rosiglitazone and pioglitazone (Table 7).

Thiazolidinediones are contraindicated in patients with type 2 diabetes mellitus and NYHA class III–IV heart failure, with elevated liver transaminases › 3 times the upper limit of normal, during pregnancy and lactation.

The results of international studies show that glitazones are effective for the treatment of type 2 diabetes. The use of rosiglitazone at a dose of 4 and 8 mg per day was accompanied by a statistically significant decrease in both the level of fasting glycemia by 0.9–2.1 mmol/l and 2–3 mmol/l, respectively, and postprandially, glycated hemoglobin decreased by 0.3 % and 0.6–0.7%, respectively. In addition, it has been demonstrated that the incidence of heart failure with thiazolidinediones is the same as in the placebo group (‹1%), in combination with insulin therapy - 1-3%, while with insulin therapy alone - 1% .

Prandial regulators (glinids)

Prandial regulators are short-acting drugs that realize their hypoglycemic properties by acutely stimulating insulin secretion, which allows effective control of glycemic levels after meals.

The mechanism of action of drugs in this group is to close ATP-sensitive K+ channels in pancreatic cells, which promotes depolarization and opening of Ca2+ channels, which increases the flow of calcium into β-cells, which, in turn, leads to insulin secretion.

It is important to note that the effect of glinides on ATP-sensitive K+ channels in the β-cell is comparable in potency to SM drugs, but these two groups of drugs realize this effect through different binding sites on the surface of the β-cell.

Two drugs of this group are registered in our country: repaglinide and nateglinide (Table 8).

α-glucosidase inhibitors

This group of drugs includes drugs that compete with dietary carbohydrates for the binding centers of gastrointestinal enzymes involved in the breakdown and absorption of carbohydrates, that is, they are competitive inhibitors.

Only one drug from this group is registered in our country - acarbose.

Under the influence of acarbose, the amount of carbohydrates absorbed does not decrease, but their absorption slows down significantly, thereby reliably preventing a sharp increase in blood sugar after meals. At the same time, the drug itself is practically not broken down and is not absorbed into the blood.

Acarbose does not stimulate insulin secretion from pancreatic β-cells, therefore it does not lead to hyperinsulinemia and does not cause hypoglycemia. Slowing down the absorption of glucose into the blood under the influence of this drug facilitates the functioning of the pancreas and protects it from overstrain and exhaustion. Acarbose has been shown to reduce insulin resistance. With long-term use, it leads to a flattening of the daily glycemic curve, a decrease in the average daily glycemic level, a decrease in the level of fasting glycemia, as well as a decrease and normalization of the level of glycated hemoglobin, which helps prevent late complications of diabetes mellitus. Treatment with acarbose begins with 50 mg during dinner, gradually increasing the dose to 300 mg per day (100 mg 3 times a day).

And finally, it should be noted the results of the use of acarbose for the prevention of type 2 diabetes mellitus - Stop NIDDM. This study demonstrated that the use of acarbose in patients with impaired glucose tolerance reduced the risk of developing type 2 diabetes by 37%.

Incretin mimetics (glucagon-like polypeptide 1 receptor agonists)

The first incretin mimetic approved by the US FDA for the treatment of patients with type 2 diabetes mellitus is exenatide (BYETTA). The mechanism of action of this drug is closely related to the main biological effects of gastrointestinal hormones - incretins. It is known that food intake stimulates the formation of many gastrointestinal hormones involved in the regulation of gastric juice secretion, pancreatic enzymes, causes contraction of the gallbladder and ensures the absorption of nutrients (Fig. 3).

The most popular and best studied at present is glucagon-like polypeptide 1 (GLP-1). GLP-1 is produced by enteroendocrine L cells of the small intestine, and its secretion from gastrointestinal endocrine cells is regulated by several intracellular signals, including protein kinase A, protein kinase C, and calcium. Numerous experimental studies have demonstrated that GLP-1 secretion is controlled by nutrients as well as neural and endocrine signals. Studies by Kieffer T.Y., 1999, Drucker D.J., 1998, Massimo S.P., 1998, showed that GLP-1 is secreted in response to the intake of mixed food and individual components such as glucose, fatty acids and dietary fiber. Thus, oral administration of glucose in humans led to a biphasic increase in plasma GLP-1, while intravenous infusions of glucose had a minimal effect. The half-life of circulating, biologically active GLP-1 is less than 2 minutes. This short plasma half-life of GLP-1 is due to the protease activity of the enzyme dipeptidyl peptidase IV (DPP-IV). Taking into account the role of gastrointestinal hormones in the regulation of carbohydrate metabolism, two new classes of drugs have been proposed: incretin mimetics and DPP-IV inhibitors.

Under the influence of exenatide, there is a glucose-dependent increase in insulin secretion, restoration of the first phase of insulin secretion, suppression of glucagon and FFA secretion, slowing down gastric emptying and reducing food intake.

Various international studies have demonstrated that the effects of exenatide are independent of the duration and severity of type 2 diabetes.

The starting dose of exenatide is 5 mcg twice daily for 60 minutes before breakfast and before dinner. After 1 month from the start of therapy, the dose can be increased to 10 mcg twice a day.

The main side effect is mild to moderate nausea, which resolves in 1–2 weeks.

Thus, this fundamentally new class of drugs is indicated for the treatment of patients with type 2 diabetes mellitus as an additional therapy to metformin, sulfonylureas, or their combination to improve glycemic control.

Dipeptidyl peptidase inhibitor-IV

Last year, a new class of oral drugs for the treatment of type 2 diabetes mellitus, the DPP-IV inhibitor, appeared on the global pharmaceutical market. The first and only member of this class recommended by the FDA is sitagliptin. The mechanism of action of this drug, as well as the action of exenatide, is closely related to the basic biological effects of hormones of the gastrointestinal tract. Sitagliptin is a powerful, fully reversible inhibitor of the DPP-4 enzyme, thereby leading to an increase in the level of active forms of incretin. The action of sitagliptin is to enhance the glucose-dependent insulin response and simultaneous suppression of glucose-dependent glucagon secretion against the background of increased blood glucose levels. Based on the results of numerous international studies of sitagliptin, the following data were obtained:

Significant and sustained reduction in fasting plasma glucose levels;

Significant reduction in postprandial fluctuations in plasma glucose levels;

Significant reduction in glycated hemoglobin levels;

Improved b-cell function.

The incidence of hypoglycemia in the studies was low and equal to that observed with placebo. Sitagliptin does not affect body weight, which is also important in the treatment of patients with type 2 diabetes and obesity. This drug has a long duration of action, so it is taken once a day.

Insulin therapy

Despite the large selection on the pharmaceutical market of various groups of oral hypoglycemic drugs that modulate various pathophysiological aspects of type 2 diabetes, it is rarely possible to achieve and maintain target glycemic values ​​for a long time. The UKPDS study confirmed that early addition of insulin therapy to oral antihyperglycemic agents can safely maintain HbA1c close to 7% in the first 6 years after diagnosis. Thus, switching to insulin therapy in type 2 diabetes mellitus to compensate for β-cell function is a logical therapeutic approach to achieve optimal glycemic control.

Experts who participated in the Consensus Statement of the American Diabetes Association and the European Association for the Study of Diabetes propose the following scheme for initiating insulin therapy in patients with type 2 diabetes (Scheme 2).

Thus, insulin therapy is indicated when diet and maximum doses of glucose-lowering drugs are ineffective (HbA1c›>7.5%, fasting glycemia >8.0 mmol/l with BMI<25 кг/м2), при наличии кетоацидоза, временный перевод на инсулинотерапию показан при оперативном вмешательстве.

Modern types of insulin are presented in table 9.

Combination therapy

For many patients with type 2 diabetes, monotherapy is usually not enough to achieve and maintain target glycemic levels over a long period of time.

The UKPDS study demonstrated the progressive course of type 2 diabetes. β-cell function is known to deteriorate at a rate of approximately 5% per year from diagnosis. This explains the decrease in the effectiveness of monotherapy, identified when assessing the number of patients who had a glycated hemoglobin level of less than 7% after 3.6 and 9 years from the start of observation. Thus, in order to maintain glycemic control and prevent the development of diabetes complications, constant strengthening of glucose-lowering therapy is necessary. Therefore, the use of combination therapy in the early and subsequent stages of the disease is considered completely justified. It should be noted that the most preferred are combinations of oral hypoglycemic drugs that affect both pathophysiological defects of type 2 diabetes mellitus (for example, metformin in combination with a sulfonylurea, sulfonylurea in combination with exenatide). The most effective combination is insulin in combination with metformin. It is important to note that combination therapy of insulin and thiazolidinediones is not currently approved in the European Union.

An important role in the treatment of patients is played by the degree of compliance with the recommendations prescribed by the doctor (compliance). Obviously, the greater the number of drugs, the lower the compliance. In this regard, pharmaceutical companies have developed fixed combination drugs. This therapy provides maximum effectiveness in achieving almost normal glycemic control: it is possible to minimize the side effects of the components of the combination due to the low dosage. All this leads to an improvement in the quality of life of patients and increases adherence to treatment.

Conclusion

In conclusion, I would like to once again emphasize the importance of achieving and maintaining target glycemic values ​​over a long period of time. Most patients at the first stage should be prescribed metformin simultaneously with recommendations on nutrition and physical activity, almost at the stage of diagnosis. If it is impossible to achieve or maintain “near-normal” glycemic values ​​using one group of drugs, combination therapy is indicated. Taking into account the results of international studies, it is recommended that insulin therapy be prescribed earlier for patients who have not achieved target glycemic values ​​using oral hypoglycemic drugs.

6. I.I.Dedov, M.V.Shestakova. Diabetes; Moscow 2003.
7. Miyazaki Y., Glass L., Triplitt C. et Al. Effect of rosiglitazone on glucose and non–esterified fatty acid metabolism in type II diabetic patients. Diabetologia, 2001, 44: 2210–2219.
8. Nesto R.W., Thiazolidinedione use, fluid retention and congestive heart failure: a consensus statement from the American heart association and American diabetes association. Diabetes care, 2004, 27: 256–263.
9. Polonsky K. Alternations in immunoreactive proinsulin and insulin clearance inducted by weight loss in NIDDM. Diabetes 1994, 43: 871–877.
10. DAlessio D.A, Vahl T.P. Glucagon-like peptide 1: evolution of an incretin into a treatment for diabetes. Am J Physiol Endocrinol Metab. 2004, 286:E882–E90.
11. Drucker DJ. Biological action and therapeutic potency of the glucagons–like peptides. Gastroenterology 2002, 122:531–544.
12. Egan J.M., Meneilly G.S., Elahi D. Effects of 1–mo bolus subcutaneous administration exentid–4 in type 2 diabetes. Am J Physiol Endocrinol Metab. 2003, 284:E1072–E1079.
13. Drucker DJ. Enhancing incretin action for the treatment of type 2 diabetes. Diabetes Care 2003, 26: 2929–2940.
14. Heine R.J., Van Gaal L.F., Johns D. et al. Exenatide versus insulin glargine in patients with suboptimally controlled type 2 diabetes. Ann Intern Med 2005, 143(8): 559–569.
15. Wright A. et al. Sulfonilurea inadequacy: efficacy of addition of insulin over 6 years in patients with type 2 diabetes mellitus in U.K. prospective Diabetes Study (UKPDS 57). Diabetes Care 2002, 25: 330–336.
16. UK Prospective Diabetes Study Group: UK Prospective Diabetes Study 16: overview of 6 years therapy of type II diabetes: a progressive disease. Diabetes 1995, 44: 1249–1258.

Non-insulin-dependent diabetes mellitus is an autoimmune disease characterized by impaired absorption of glucose, with its accumulation in the blood.

New techniques

Modern technologies for treating the disease make it possible to eliminate the cause of diabetes and alleviate the patient’s condition. Their action is aimed at the proper functioning of the glucose-insulin connection.

Anti-hyperglycemia patch

This method of dealing with high glucose is popular among Internet users. The patch is impregnated with a special hormonal solution and is not a means of combating diabetes, but a preventive measure.

According to reviews, the patch helps burn subcutaneous fatty tissue, which primarily disrupts the functioning of the pancreas. The idea belongs to Chinese developers.

Medicines

The latest developments by doctors have made it possible to obtain drugs against increased glucose and its forced distribution. These drugs include pioglitazones and rosiglitazones. The main effect of medications: irritation of insulin receptors to prevent the sedimentation of sugar in the blood.

The most popular means are:

• Aktos;
• Roglit;
• Pioglar;
• Amaryl.

The maximum dosage per day is no more than 45 mg, and the average norm is 30 mg. The reception is made once.

Contraindications for use are:

• pregnancy;
• insulin-dependent form of pathology;
• acute liver failure;
• age less than 18 years.

Medicines are not insulin substitutes, they just stimulate its production. Side effects due to antidiabetic therapy with modern medications cannot be ruled out.

Mitochondrial uncoupling

The essence of the treatment: the destruction of fatty acids and sugar by enhancing mitochondrial energy. For enhanced combustion, an artificially derived drug approved by the All-Russian Health Organization is used. Fat depletion occurs in an intracellular manner.

Taking the modified medication allows you to burn calories and keep your weight under control, which in turn triggers the process of producing normal pancreatic hormone.

New trend in endocrinology. In Russia, approval for such a treatment for diabetes has not yet been received, but the method has been practiced abroad for a long time. The technique using stem cells is aimed not only at stimulating insulin synthesis, but also at eliminating pathologies in the functioning of the pancreas.

Stem cells are a universal aid for restoring an organ or system that has lost its basic functions. Therapy is carried out in several stages:

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1. Seeking medical help and collecting biological material.
2. Preparation of the obtained material: laboratory research, genetic reproduction.
3. Implantation of stem cells (own, but with an implanted genome, and new stem cells for tissue regeneration).

The procedure is accompanied by minimal risk; this is associated with the individual characteristics of the patient’s body.

The use of a magnet helps saturate the patient’s body with oxygen. The work of the endocrine system is enhanced and the release of adrenal hormones (adrenaline and thyroxine) is activated. The procedure is effective only for type 2 diabetes, since the functioning of biochemical metabolic processes in the body improves.

The method is not approved for use in pregnant women and nursing mothers, as well as in persons diagnosed with tuberculosis. Low blood pressure and increased temperature are temporary contraindications.

Cellulose

The use of fiber is not so much a new way to combat diabetes as maintenance therapy. Consumption of fiber affects the acceleration of carbohydrate metabolism, during which glucose is absorbed, breakdown products and toxins are removed from the intestines, weight is normalized and excess fluid is absorbed. Fiber contains plant cellulose.

Traditional treatment or new methods?

The choice of therapy should be entrusted to a professional. Endocrinologists advise that before using both traditional and modern methods of treatment, undergo a full examination, identify the cause of the pathology, and then treat it.

Conventional treatment for type 2 diabetes is as follows:

• changing your diet and introducing physical activity;
• drug hypoglycemic therapy;
• insulin therapy.

Treatment with traditional means has been used for a long time. The medication contains metformin in the form of hydrochloride. The therapeutic effect is due to a decrease in the concentration of glucose in serum and plasma, while metformin has no effect on insulin.

The main goal of hypoglycemic drugs is to maintain acceptable sugar levels. To improve the condition of the pancreas, decoctions of medicinal plants are taken, as well as enzyme therapy.

Compared to new technologies and medications, traditional methods are less effective, as they require periodic repetitions in the treatment of diabetes. However, in most cases, traditional therapy is still used.

The advantage of new methods is the elimination of the disease for a long time. Some patients who received stem therapy noted the absence of signs of diabetes for several years, but they followed the recommended diet and regularly did exercises.

Not all modern methods are used in the Russian Federation; some of them, such as cell therapy, are not officially carried out in the country. Other methods may not be effective in diagnosing insulin-dependent diabetes. The disadvantage is the inflated cost, which is inaccessible to ordinary citizens.

Preventive measures include following a diet and maintaining the necessary physical activity. Diabetes mellitus type 2 occurs in middle-aged and elderly people. For this category of citizens, a set of physical exercises and a special diet with a minimum amount of carbohydrates are being developed.

Medicines and herbal infusions are also used for prevention purposes.

According to statistics, many patients with type 2 diabetes are overweight, and they are also elderly people.

Only 8% of patients have normal body weight.

As a rule, a person is diagnosed with a combination of two or more risk factors for developing the disease.

Let's consider the factors that increase the risk of the onset of the disease:

1. Genetic predisposition. If one of the parents has T2DM, the probability of inheritance is 30%, and if both parents are sick, then the risk increases to 60%. Increased sensitivity to a substance that enhances insulin production, which is called enkephalin, is inherited.
2. Obesity, excess body weight, abuse of harmful products.
3. Traumatic damage to the pancreas.
4. Pancreatitis, causing damage to beta cells.
5. Frequent stress, depression.
6. Insufficient physical activity, predominance of adipose tissue over muscle.
7. Transferred viruses(chickenpox, mumps, rubella, hepatitis) - provoke the development of the disease in people with a hereditary predisposition.
8. Chronic diseases.
9. Old age (over 65 years old).
10. Hypertonic disease and increased concentration of triglycerides in the blood due to overuse of fatty foods.

Diagnostic methods

In persons who fall under one of the risk factors listed above, a set of laboratory tests is carried out to allow timely identification of the disease.
If you are at risk, you need to be tested once a year.

If suspected, the following tests are prescribed:

• determination of glucose concentration in capillary blood;
• glucose tolerance - a test for early detection of the disease;
• glycated hemoglobin in the blood.

A blood test for type 2 diabetes is positive if:

• the level of glucose in capillary blood exceeds 6.1 mmol/l;
• when testing for tolerance, 2 hours after taking glucose, its level is more than 11.1 mmol/l; if the glucose level is in the range of 7.8-11.1 mmol/l, a diagnosis is made, which requires further examination under the supervision of a therapist;
• with a glycated hemoglobin content of 5.7%, a person is considered healthy, a concentration of more than 6.5% - the diagnosis is confirmed, intermediate values ​​- a high risk of development.

When are injections necessary?

In severe cases of the disease, insulin injections are prescribed along with medications. Thus, this form of the disease can become insulin dependent, making life much more difficult.

Depending on how capable the body is of compensating for carbohydrate metabolism disorders, There are three stages of the disease:

1. Reversible (compensatory).
2. Partially reversible (subcompensatory)
3. Carbohydrate metabolism is irreversibly impaired - the stage of decompensation.

Symptoms

There are many cases when the disease is detected by chance, during a routine examination, during a blood sugar test. More often, symptoms appear in overweight people and those who have crossed the 40-year mark.

Associated symptoms:

• frequent bacterial infections due to decreased immunity;
• limbs lose normal sensitivity;
• Poorly healing ulcers and erosive formations appear on the skin.

Treatment

Is there a cure for type 2 diabetes? Every sick patient asks this question.
Existing standards for the treatment of type 2 diabetes mellitus consider the main principle to be the achievement of the following goals:

• elimination of symptoms;
• decreased blood sugar levels;
• control of metabolism;
• warning ;
• ensuring the highest possible standard of living;

1. Diet;
2. Recommended physical activity;
3. Self-monitoring of the patient’s condition;
4. Teaching the patient skills to live with diabetes.

If diet therapy is ineffective, then additional drug therapy is prescribed.

Drug treatment of type 2 diabetes mellitus: drugs that lower sugar

Modern pharmacotherapy for diabetes mellitus 2 offers many different drugs that lower sugar. Prescription of medications is carried out based on laboratory parameters and the general condition of the patient. The severity of the disease and the presence of complications are taken into account.

Groups of medications prescribed to patients with type 2 diabetes to lower blood sugar (glucose) levels:

1.Sulfonylurea derivatives– have a double effect: they reduce cell resistance to insulin and increase its secretion.
In some cases, they can sharply reduce blood sugar levels.
Prescribed drugs: glimeperide, chlorpropamide and glibenclamide, etc.

2. Biagunids. Increases the sensitivity of muscle tissue, liver and fatty tissue to insulin.
They reduce weight, normalize lipid profile and blood viscosity.
The drug Metformin is prescribed, but it causes side effects, stomach and intestinal disorders, as well.

3. Thiazolidinone derivatives reduce glucose levels, increasing the sensitivity of cell receptors and normalize the lipid profile.
The medications prescribed are rosiglitazone and troglitazone.

4. Incretins improve the function of pancreatic beta cells and insulin secretion, inhibit the release of glucagon.
The drug prescribed is glucagon-like peptide-1.

5. Dipeptidyl peptidiase inhibitors 4 improve glucose-dependent insulin release by increasing the susceptibility of pancreatic beta cells to the entry of glucose into the blood.
The medications prescribed are vildagliptin and sitagliptin.

6. Alpha-glucosidase inhibitors disrupt the absorption of carbohydrates in the intestines, reduce the concentration of sugar and the need for injections.
Miglitol and acarbose are prescribed.

IMPORTANT!

Drugs that lower blood sugar levels are prescribed exclusively by the attending physician, since self-medication in this situation is life-threatening. The list of drugs is for informational purposes only.

Combination therapy involves prescribing 2 or more medications at the same time. This type has fewer side effects than taking one drug in a large dosage.

Modern methods of treating type 2 diabetes mellitus

Modern treatment of type 2 diabetes requires doctors to achieve the following goals:

• stimulate insulin production;
• reduce tissue immunity (resistance) to insulin;
• reduce the rate of synthesis of carbohydrate compounds and slow down the process of its absorption through the intestinal wall;
• correct the imbalance of lipid fractions in the bloodstream.

At first, only 1 drug is used. Subsequently, several are combined. If the disease progresses, the patient’s condition is poor and previous medications are ineffective, insulin therapy is prescribed.

Physiotherapy and ozone therapy

• increases the permeability of cell membranes, which increases the flow of carbohydrates into tissues and eliminates the lack of energy, while reducing protein breakdown;
• activates glucose metabolism in red blood cells (erythrocytes), which increases the saturation of tissues with oxygen;
• strengthens the vascular wall;
• especially effective for coronary heart disease and atherosclerosis in elderly patients.

But there are also disadvantages to ozone therapy: it can suppress the patient’s immunity, which can provoke the development of chronic infections and pustular skin lesions.

The course of treatment is up to 14 procedures, involving intravenous administration of saline solution that has undergone ozonation. Enemas with an ozno-oxygen mixture are also used.

The following physiotherapy procedures are used for diabetes:

• electrophoresis;
• magnetic therapy;
• acupuncture;
• hydrotherapy;
• physical therapy.

How to treat type 2 diabetes with nutrition?

Treatment regimens for type 2 diabetes mellitus using diet are based on the following principles:

• exclusion of refined carbohydrates (jams, desserts and honey) from the diet;
• fat intake should correspond to 35% of the daily requirement;
• counting the number of bread units and bringing your diet in line with the doctor’s recommendations.

Many patients have some degree of obesity, and therefore, by achieving weight loss, it is possible to achieve a decrease in glycemia (glucose), which often eliminates the need for drug treatment of the disease.

Diet therapy is the main part of treatment. The proportion of proteins in the diet should be 20%, fats -30% and carbohydrates 50%. It is recommended to divide meals into 5 or 6 times.

Fiber in the diet

A prerequisite for a therapeutic diet is the presence of fiber.
Rich in fiber:

Including guar, fiber and pectin in the diet gives excellent results. The recommended dosage is 15 grams per day.

What is a bread unit

The practical significance of the bread unit is that it can be used to determine the dose of injection for oral administration. The more bread units consumed, the larger the dose is administered to normalize glucose levels in the body.

For the error-free calculation of XE, many special tables have been compiled containing a list of food products allowed for patients with diabetes and the correspondence of the indicated units to them.

Folk remedies

Folk remedies can be considered as an addition to the main therapy.

A noticeable effect is observed a month after systematic use.

IMPORTANT!

Before starting to use various herbal infusions, the patient is recommended to consult a doctor, since the use of some herbs has contraindications for various conditions.

Useful video

What treatment methods are considered the most effective? Watch the video:

Goals of therapy

The main goal of treating type 1 and type 2 diabetes mellitus is to preserve the patient’s quality of life and normalize metabolism. It is important to prevent the development of complications, to adapt a person to life taking into account this complex diagnosis. Proper treatment only delays the onset of serious consequences.