Content

Treatment of type 2 diabetes prescribed after diagnosis (which, unlike type 1 diabetes, is not insulin-dependent) provides a wide range of methods, consisting of both traditional recipes and medications. The main emphasis is on changing lifestyle in terms of diet. Medical practice shows that this therapeutic approach often produces positive results, provided that the patient conscientiously follows all recommendations.

What is type 2 diabetes

Type 2 diabetes is an endocrine disease in which the body's tissues are sensitive to the action of insulin. The high productivity of pancreatic β-cells provoked by the disease depletes the cell resource, insulin production begins to decrease, which leads to the need for its injections. The disease often begins after 40 years of age. The occurrence of the disease is caused only by lifetime health disorders and does not depend on genetic disorders. Most patients have an increased body mass index.

Treatment

Diabetes is one of those types of diseases in the treatment of which identifying the cause of the disease plays an important role. Against the background of drug therapy, a prerequisite is the restructuring of the patient’s lifestyle, especially in terms of giving up bad habits. The consumption of foods with a high glycemic index (the ability to increase blood sugar) should be reduced. The general treatment regimen for diabetes is approximately the same for men, women, children and the elderly.

It is recommended to reduce the level of animal fats and simple carbohydrates in your diet. Meals should be regular and in small portions. It is necessary to get an idea of ​​energy expenditure during the day and, depending on this, plan the caloric intake of food. If you have a sedentary lifestyle, you should not eat a bowl of soup and a frying pan of potatoes with meat, washing it all down with sweet tea. You should not neglect medications if they are prescribed. Physical activity in the form of jogging or swimming is indicated.

Main goals of therapy

Treatment begins with the use of one drug and gradually switches to several, and then, if necessary, to insulin. Comprehensive therapy for type 2 diabetes is designed to attack the disease from several directions:

1. Therapy should enhance insulin production and lead to compensation for diabetes.
2. It is necessary to reduce the degree of insulin resistance of body tissues.
3. Slow down the synthesis of glucose and its absorption from the gastrointestinal tract into the blood.
4. Bring the proportion of lipids in the blood closer to normal (dyslipidemia).

Treatment of type 2 diabetes without drugs

It is beneficial for pharmaceutical companies to support the idea that chronic diabetics must take insulin injections and medications to normalize their sugar levels throughout their lives. But insulin and “chemistry” have their side effects. Therefore, cure without drugs is becoming increasingly important. There are several known methods of drug-free therapy:

1. Switch to a low-carbohydrate diet and increase the frequency of meals.
2. Herbal medicine recipes aimed at bringing plants and roots that reduce sugar levels to the maximum possible in the diet.
3. Acupuncture. Regulates insulin production, improves blood counts.
4. Physical activity helps burn glucose in the blood.

Physiotherapy

The use of various physical factors (light, radiation, heat and others) has proven medical effectiveness. The following methods are practiced:

1. Electrophoresis. Drugs that have a therapeutic effect on the body are introduced into the body through the skin. Diabetics are prescribed electrophoresis with magnesium.
2. Magnetotherapy. Using special equipment, the area of ​​the pancreas is exposed to a magnetic field.
3. Oxygenation. The method involves pumping oxygen inside a special chamber. Effective for hypoxia in diabetics.
4. Plasmapheresis. Represents blood purification. Indicated for diabetics with renal failure and septic intoxication.
5. Ozone therapy. During therapy, cell permeability to glucose increases and blood sugar decreases.

Physical exercise

Therapeutic exercise allows you to burn excess glucose in the blood, reduce body weight, and increase blood flow to the muscles. If you have diabetes, your doctor may recommend exercises:

1. Walking in place: raising your knees high, march in place for 2-4 minutes.
2. Steps: Stand up straight with your arms down. Next, step back with your left foot, raise your arms and inhale at the same time. Next, exhale, lower your arms, and take a straight stance.
3. Bends: Stand up straight and touch your toes one at a time.

Folk remedies

Diabetes has been known since ancient times and traditional medicine has developed many methods and recipes to combat the disease. Folk remedies for type 2 diabetes:

1. Nettle: pour boiling water over freshly picked leaves and leave for 8 hours, strain and consume a quarter glass three times a day before meals.
2. Horsetail: collect the stems, add boiling water and cook for 5 minutes. Leave for two hours. Take half a glass twice a day before meals.
3. Dandelion root: brew two tablespoons of dried roots in 0.5 liters of boiling water and leave for 4 hours. Take half a glass before meals, twice a day. Treatment of type 2 diabetes mellitus with folk remedies should be carried out after consultation with a doctor.

Treatment of type 2 diabetes mellitus with drugs

A doctor will help you select effective glucose-lowering drugs for the treatment of type 2 diabetes, based on the severity of the disease and the presence of complications in the patient. Popular groups of medications are:

1. Sulfonylureas – Glimepiride, Chlorpropamide. They stimulate the secretion of pancreatic hormone, reducing the resistance of peripheral tissues to insulin.
2. Biguanides – Metformin, increases the sensitivity of liver tissue and muscles to insulin, which leads to weight loss and improved fat metabolism.
3. Thiazolidinedione derivatives – Troglitazone, Rosiglitazone. They increase the activity of insulin receptors, reducing glucose levels.
4. Alpha-glucosidase inhibitors - Acarbose, Miglitol - interfere with the absorption of carbohydrates in the gastrointestinal tract, reducing hyperglycemia.
5. Dipeptidyl peptidase inhibitors – Sitagliptin, causes an increase in the sensitivity of pancreatic cells.

Vipidia

An oral hypoglycemic drug is Vipidia, which improves metabolic control of plasma glycemia. The medication can be used in monotherapy or with other drugs, including insulin. Contraindications for the use of Vipidia include hypersensitivity to alogliptin, ketoacidosis, liver and kidney disorders, pregnancy, and poor health. The therapeutic dose of the drug is 25 mg once a day, regardless of food intake.

Diapil

Dietary supplements (BAA) used in the treatment of type 2 diabetes mellitus include the natural remedy Diapil. It is prescribed to lower blood sugar levels, normalize carbohydrate metabolism and prevent the development of complications of diabetes mellitus. The composition of the dietary supplement includes andrographis herb extract, which has an anti-inflammatory and tonic effect. According to reviews from patients who took Diapil, the drug reduces the need for insulin.

The most effective treatment for type 2 diabetes

Drug treatment of type 2 diabetes mellitus includes the following effective drugs based on metformin:

1. The drug Glucophage is an original long-acting medication, taken at night, effective after 10 hours. The effect of taking it is lower fasting glucose in the morning.
2. Siofor is a cheap analogue of Glucophage and can be used to prevent the development of type 2 diabetes. Take metformin 1-2 tablets twice a day. The drug takes effect within half an hour. The dose is increased gradually so that acidosis does not develop.

New in the treatment of type 2 diabetes

To date, scientists and doctors have developed or are conducting research to find new methods of treating type 2 diabetes:

1. A low-carb diet combined with physical activity often works better than pills.
2. Groups of drugs that remove excess sugar through the kidneys.
3. Injections with stem cells obtained from the umbilical cord of newborns.

Diet

To control blood sugar levels, you need to follow a certain diet. It involves calculating the glycemic index (GI). Products with a low level of carbohydrates are allowed to be eaten with virtually no restrictions, while products with a high level are strictly prohibited. An approximate list of allowed and prohibited foods:

	Authorized Products	Prohibited
	Garlic, onions, tomatoes, all types of cabbage, cucumbers, green beans, turnips	Canned sweet corn, beets, potatoes, pumpkin
	Cherry, strawberry
	Apricots, grapefruit, plums, apples,	Melon, bananas, pineapples
	Barley, peas, lentils, corn, bulgur, oatmeal, buckwheat	Semolina, muesli, instant porridge
Sweets	Fructose, dark chocolate,	Raisins, milk chocolate, bars, sugar, waffles
	Mushrooms, rice bran, bread, natural spaghetti	Buns, biscuits, pasta, cookies, brown bread, wheat flour, dumplings, sauces, spices
Dairy		Cheese, full-fat milk, animal fats
	Chicken, rabbit. lean veal or beef, quail eggs	Red fatty meat, sausages, fatty salted fish, smoked meats
	Natural juices	Sweet carbonated drinks, beer, wine, kvass

Benefits of fiber for diabetics

When food containing simple carbohydrates enters the body, they are instantly transformed into sugar. In diabetes mellitus, glucose is produced that is poorly absorbed, leading to a malfunction of the pancreas. If complex carbohydrates (fiber, starch, pectins) are consumed, then absorption slows down, breakdown into glucose does not occur, and the person remains full longer.

Dietary fiber is extremely important in a diabetic diet because it lowers blood glucose levels. When consuming, you should adhere to the rule of 25-40 g of fiber daily; intake should be slow so that the body can process the food completely and does not overload the intestines. Soluble fiber lowers cholesterol levels, slows down the digestion of sugar, and serves as a preventive measure for vascular pathologies. The insoluble type has zero calories and lowers blood pressure and homocysteine ​​levels.

Carbohydrates for type 2 diabetes

The diet of a person with type 2 diabetes should include carbohydrates because they provide energy to the body, but it is important to remember that there are different types of carbohydrates. The most beneficial for a diabetic are considered to be complex ones - fiber, dietary fiber, and the harmful ones are simple ones, which instantly cause a “jump” in glucose. Patients with diabetes should adhere to a low-carbohydrate diet, which does not allow sugar levels to rise, reducing the risk of severe hypoglycemia.

Prevention

To prevent type 2 diabetes from developing into insulin-dependent diabetes, or to prevent the development of the disease in general, the following preventive measures are used:

• carry out nutritional correction;
• stick to a low-carbohydrate diet, take vitamins;
• be physically active;
• undergo annual screening if you are predisposed to the disease;
• stop smoking, drinking alcohol;
• maintain normal weight and prevent obesity.

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Attention! The information presented in the article is for informational purposes only. The materials in the article do not encourage self-treatment. Only a qualified doctor can make a diagnosis and give treatment recommendations based on the individual characteristics of a particular patient.

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Treatment of type 2 diabetes - medications, folk remedies and diet

Diabetes mellitus (DM) type 2 is a common non-infectious chronic disease. It affects both men and women, most often over the age of 40. The danger of type 2 diabetes is underestimated by many, and some patients, in fact, are simply not informed that they are susceptible to the disease. And those patients who are aware of their pathology often do not know what diabetes mellitus is, what it threatens, and are not aware of its danger. As a result, type 2 diabetes can become severe and lead to life-threatening conditions. Meanwhile, adequate treatment and proper nutrition for type 2 diabetes can stop the development of the disease.

Causes

When a person develops diabetes mellitus, the reasons for this fact can be varied. The second type of disease often results from:

• improper diet;
• lack of physical activity;
• excess weight;
• heredity;
• stress;
• self-medication with medications, for example, glucocorticosteroids.

In fact, there is often not just one prerequisite, but a whole complex of reasons.

If we consider the occurrence of the disease from the point of view of pathogenesis, then type 2 diabetes mellitus is caused by a relative lack of insulin in the blood. This is the name of the condition when the insulin protein produced by the pancreas becomes inaccessible to insulin receptors located on cell membranes. As a result, cells are deprived of the ability to absorb sugar (glucose), which leads to a lack of supply of glucose to the cells, as well as, no less dangerous, to the accumulation of glucose in the blood and its deposition in various tissues. According to this criterion, non-insulin-dependent diabetes mellitus differs from type 1 diabetes, in which the pancreas does not produce enough insulin.

Symptoms

Signs of the disease largely depend on the stage of the disease. In the first stages, the patient may not feel any serious discomfort, with the exception of increased fatigue, dry mouth, increased thirst and appetite. This condition is usually attributed to poor diet, chronic fatigue syndrome, and stress. However, in fact, the cause is a hidden pathology. As the disease progresses, symptoms may include:

• poor wound healing,
• weakening of the immune system,
• pain and swelling in the limbs,
• headache,
• dermatitis.

However, patients often do not correctly interpret even a set of such symptoms, and diabetes develops unchecked until it reaches intractable stages or leads to life-threatening conditions.

Diabetes mellitus type 2, treatment

In fact, there are no sufficiently effective methods to increase the uptake of glucose by cells, so the main emphasis in treatment is on reducing the concentration of sugar in the blood. In addition, efforts should be aimed at reducing the patient's excess weight, bringing it back to normal, since the abundance of adipose tissue plays an important role in the pathogenesis of diabetes.

The main factor influencing the likelihood of developing complications in type 2 diabetes is lipid metabolism disorder. An excess amount of cholesterol different from the norm can lead to the development of angiopathy.

Treatment methods

Type 2 diabetes mellitus is a disease that requires long-term and persistent therapy. In fact, all applied methods are divided into three groups:

• taking medications,
• diet,
• lifestyle change.

Effective treatment of type 2 diabetes mellitus involves fighting not only diabetes mellitus itself, but also concomitant diseases, such as:

• obesity,
• hypertension,
• angiopathy,
• neuropathy,
• depression.

Type 2 diabetes mellitus is treated on an outpatient basis and at home. Only patients with hyperglycemic and hyperosmolar coma, ketoacidosis, severe forms of neuropathies and angiopathy, and strokes are subject to hospitalization.

Medicines against diabetes mellitus

Essentially, all medications are divided into two main groups - those that affect insulin production and those that do not.

The main drug of the second group is metformin from the biguanide class. This drug is most often prescribed for type 2 diabetes. Without affecting pancreatic cells, it maintains blood glucose at normal levels. The drug does not threaten a critically low decrease in glucose levels. Metformin also burns fat and reduces appetite, which leads to a reduction in the patient’s excess weight. However, an overdose of the drug can be dangerous, as a severe pathological condition with a high mortality rate can occur - lactic acidosis.

Typical representatives of another group of drugs that affect insulin production are sulfonylurea derivatives. They directly stimulate the beta cells of the pancreas, causing them to produce insulin in increased quantities. However, an overdose of these drugs threatens the patient with a hypoglycemic crisis. Sulfonylurea derivatives are usually taken together with metformin.

There are other types of drugs. A class of drugs that enhance glucose-dependent insulin production include incretin mimetics (GLP-1 agonists) and DPP-4 inhibitors. These are new drugs, and so far they are quite expensive. They suppress the synthesis of the sugar-increasing hormone glucagon and enhance the effect of incretins - gastrointestinal hormones that increase insulin production.

There is also a drug that prevents the absorption of glucose in the gastrointestinal tract - acarbose. This remedy does not affect insulin production. Acarbose is often prescribed prophylactically to prevent diabetes.

There are also medications that increase the excretion of glucose in the urine, and drugs that increase the sensitivity of cells to glucose.

Medical insulin is rarely used in the treatment of type 2 diabetes mellitus. Most often it is used when therapy with other drugs is ineffective, in a decompensated form of diabetes mellitus, when the pancreas is depleted and cannot produce enough insulin.

Type 2 diabetes is also often accompanied by concomitant diseases:

• angiopathy,
• depression,
• neuropathies,
• hypertension,
• lipid metabolism disorders.

If such diseases are detected, then drugs are prescribed to treat them.

Types of drugs for the treatment of type 2 diabetes mellitus

Type	mechanism of action	examples
Sulfonylurea derivatives	stimulation of insulin secretion	glibenclamide, chlorpropamide, tolazamide
Glinids	stimulation of insulin secretion	repaglinide, nateglinide
Biguanides		metformin
Glitazones	decreased liver glucose production and tissue resistance to glucose	pioglitazone
Alpha-glucosidase inhibitors	slower absorption of glucose in the intestine	acarbose, miglitol
Glucanagon-like peptide receptor agonists		exenatide, liraglutide, lixisenatide
Gliptins (dipeptidyl peptidase-4 inhibitors)	glucose-dependent stimulation of insulin secretion and reduction of glucagon secretion	sitagliptin, vildagliptin, saxagliptin
Insulins	increased glucose utilization	Insulin

Diet

The essence of changing the diet for diabetes is the regulation of nutrients entering the gastrointestinal tract. The required nutrition should be determined by the endocrinologist individually for each patient, taking into account the severity of diabetes, concomitant diseases, age, lifestyle, etc.

There are several types of diets used for non-insulin-dependent diabetes (table No. 9, low-carbohydrate diet, etc.). All of them have proven themselves well and differ from each other only in some details. But they agree on the basic principle - the norms of carbohydrate consumption during illness should be strictly limited. First of all, this applies to products containing “fast” carbohydrates, that is, carbohydrates that are very quickly absorbed from the gastrointestinal tract. Fast carbohydrates are found in refined sugar, jams, confectionery, chocolate, ice cream, desserts, and baked goods. In addition to reducing the amount of carbohydrates, it is necessary to strive to reduce body weight, since increased weight is a factor that aggravates the course of the disease.

Other information

It is recommended to increase your water intake to replenish fluid loss due to frequent urination, which often accompanies diabetes. At the same time, it is necessary to completely abandon sweet drinks - cola, lemonade, kvass, juices and tea with sugar. In fact, you can only drink drinks that do not contain sugar - mineral and plain water, unsweetened tea and coffee. It must be remembered that drinking alcohol can also be harmful - due to the fact that alcohol disrupts glucose metabolism.

Meals should be regular - at least 3 times a day, and best of all - 5-6 times a day. You should not sit down at the dinner table immediately after exercise.

How to monitor your blood glucose levels

The essence of diabetes therapy is self-control on the part of the patient. With type 2 diabetes, the sugar level should be within the normal range, or close to it. Therefore, the patient needs to control his sugar level independently in order to avoid critical increases. To do this, it is advisable to keep a diary in which the values ​​of glucose concentration in the blood will be recorded. Glucose measurements can be taken with special portable glucometers equipped with test strips. It is advisable to carry out the measurement procedure every day. The optimal time for measurement is early morning. Before the procedure, you are prohibited from eating any food. If possible, the procedure can be repeated several times a day and determine the sugar level not only in the morning on an empty stomach, but also after meals, before bed, etc. Knowing the schedule of changes in blood glucose, the patient will be able to quickly adjust his diet and lifestyle so that the glucose level is in a normal state.

However, the presence of a glucometer does not relieve the patient of the need to regularly check blood sugar levels in the outpatient clinic, since the values ​​​​obtained in the laboratory are more accurate.

It's not that difficult to control your sugar levels when consuming food - after all, most products bought in the store indicate their energy value and the amount of carbohydrates they contain. There are diabetic analogs of regular foods in which carbohydrates are replaced with low-calorie sweeteners (sorbitol, xylitol, aspartame).

Fasting blood sugar level

Fruits and vegetables

Is it possible to eat fruits and berries with type 2 diabetes? Preference should be given to vegetables that contain large amounts of indigestible, but beneficial for digestion, fiber and less sugar. However, many vegetables, such as potatoes, beets and carrots, contain large amounts of starch, so their consumption should be limited. Fruits can be consumed in moderation, and only those that do not contain very high amounts of carbohydrates. Among fruits, the record holders for carbohydrate content are bananas, followed by grapes and melons. They are not recommended to be consumed as they can increase sugar levels.

Folk remedies

Folk remedies involve taking decoctions of medicinal herbs. Such therapy can not only reduce blood glucose levels, but also reduce appetite and reduce excess weight. However, folk remedies can only be taken in addition to taking medications and in consultation with your doctor.

Physical exercise

An auxiliary method of therapy is physical exercise. When performing moderate-intensity exercise, the body burns large amounts of glucose. Metabolism returns to normal and the cardiovascular system is strengthened. It is necessary to do physical exercise every day. However, the exercises should not be exhausting, since this can only achieve the opposite effect. When you are very tired, your appetite increases, and eating a lot of food can negate all the positive effects of physical activity. Fatigue triggers stress and the release of adrenal hormones, which increases blood glucose levels. Therefore, it is recommended to select the type of physical activity that would suit the patient’s athletic form - simple exercises, exercises with dumbbells or walks, jogging, swimming, cycling.

Energy costs for various types of activities

Forecast

In severe cases, when type 2 diabetes reaches the stage of decompensation, it is, as a rule, impossible to reverse the disease and return glucose levels to normal due to the depletion of the resources of the pancreas and the body as a whole. Therefore, type 2 diabetes mellitus in such a situation is an incurable disease. However, proper treatment of type 2 diabetes can extend the patient's life for many years. At the initial stage of type 2 diabetes mellitus, it is possible to control the concentration of glucose in the blood and maintain it within acceptable limits only by changing the diet and lifestyle, and increasing physical activity. As a result, the patient can live for many decades without experiencing any complications from diabetes.

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Basic principles of treatment of type 2 diabetes mellitus (DM2):

• training and self-control;
• diet therapy;
• dosed physical activity;
• tableted glucose-lowering drugs (TSD);
• insulin therapy (combined or monotherapy).

Drug therapy for T2DM is prescribed in cases where dietary measures and increased physical activity for 3 months do not allow achieving the treatment goal for a particular patient.

The use of TSP, as the main type of hypoglycemic therapy for type 2 diabetes, is contraindicated in:

• the presence of all acute complications diabetes mellitus (SD);
• severe damage to the liver and kidneys of any etiology, occurring with disruption of their function;
• pregnancy;
• childbirth;
• lactation;
• blood diseases;
• acute inflammatory diseases;
• organic stage of vascular complications of diabetes;
• surgical interventions;
• progressive loss of body weight.

The use of TSP is not recommended in persons with long-term inflammatory processes in any organ.

Pharmacotherapy for type 2 diabetes mellitus is based on the impact on the main pathogenetic links of this disease: impaired insulin secretion, the presence of insulin resistance, increased glucose production in the liver, glucotoxicity. The action of the most common tableted glucose-lowering drugs is based on the inclusion of mechanisms that make it possible to compensate for the negative impact of these pathological factors (The treatment algorithm for patients with type 2 diabetes is presented in Fig. 9.1).

Figure 9.1. Treatment algorithm for patients with T2DM

In accordance with the application points, TSP actions are divided into three main groups:

1) Enhancing insulin secretion: stimulators of the synthesis and/or release of insulin by B cells - sulfonylurea drugs (SMU), non-sulfonylurea secretagogues (glinides).
2) Reducing insulin resistance (increasing insulin sensitivity): suppressing increased liver glucose production and increasing glucose utilization by peripheral tissues. These include biguanides and thiazolindiones (glitazones).
3) Suppressing the absorption of carbohydrates in the intestine: a-glucosidase inhibitors (Table 9.1.).

Table 9.1. Mechanism of action of oral glucose-lowering drugs

Currently, these groups of drugs include:

1. 2nd generation sulfonylureas:

• glibenclamide (Maninil 5 mg, Maninil 3.5 mg, Maninil 1.75 mg)
• Gliclazide (Diabeton MV)
• glimepiride (Amaryl)
• gliquidone (Glurenorm)
• glipizide (Glibenez-retard)

2. Nonsulfonylurea secretagogues or prandial glycemic regulators (glinides, meglitinides):

• repaglinide (Novonorm)
• nateglinide (Starlix)

3. Biguanides:

• metformin (Glucophage, Siofor, Formin Pliva)

4. Thiazolidinediones (glitazones): sensitizers that can increase the sensitivity of peripheral tissues to the action of insulin:

• Rosiglitazone (Avandia)
• pioglitazone (Actos)

5. α-glucosidase blockers:

• acarbose (Glucobay)

Sulfonylureas

The mechanism of the hypoglycemic effect of PSM is to enhance the synthesis and secretion of insulin by B-cells of the pancreas, reduce neoglucogenesis in the liver, reduce the release of glucose from the liver, and increase the sensitivity to insulin of insulin-dependent tissues as a result of the effect on receptors.

Currently, second generation PSMs are used in clinical practice, which have a number of advantages compared to first generation sulfonylurea drugs (chlorpropamide, tolbutamide, carbutamide): they have higher hypoglycemic activity, have fewer side effects, interact less frequently with other drugs, and are available in more convenient form. Indications and contraindications for their use are presented in table. 9.2.

Table 9.2. Indications and contraindications for taking medications

PSM therapy begins with a single dose before breakfast (30 minutes before meals) in the smallest dose, if necessary, gradually increasing it with an interval of 5-7 days until the desired reduction in glycemia is obtained. A drug with faster absorption (micronized glibenclamide - maninil 1.75 mg, maninil 3.5 mg) is taken 15 minutes before meals. It is recommended to start treatment of TSP with milder drugs, such as gliclazide (diabeton MB) and only subsequently switch to more powerful drugs (Maninil, Amaryl). PSM with a short duration of action (glipizide, gliquidone) can be immediately prescribed 2-3 times a day (Table 10).

Glibenclamide (Maninil, Betanaz, Daonil, Euglucone) is the most commonly used sulfonylurea drug. It is completely metabolized in the body with the formation of active and inactive metabolites and has a dual excretion route (50% through the kidneys and a significant part through the bile). In the presence of renal failure, its binding to proteins decreases (with hypoalbuminuria) and the risk of developing hypoglycemia increases.

Table 10. Characteristics of doses and administration of PSM

Glipizide (glibenez, glibenez retard) is metabolized in the liver to form inactive metabolites, which reduces the risk of hypoglycemia. The advantage of sustained release glipizide is that the release of its active substance is constant and does not depend on food intake. An increase in insulin secretion when used occurs mainly in response to food intake, which also reduces the risk of hypoglycemia.

Glimepiride (amaryl)- a new tableted glucose-lowering drug, which is sometimes referred to as the third generation. It has 100% bioavailability and causes the selective selection of insulin from B cells only in response to food intake; does not block the decrease in insulin secretion during exercise. These features of the action of glimepiride reduce the likelihood of hypoglycemia. The drug has a dual route of elimination: with urine and bile.

Gliclazide (diabeton MB) is also characterized by absolute bioavailability (97%) and is metabolized in the liver without the formation of active metabolites. The prolonged form of gliclazide - Diabeton MB (a new modified release form) has the ability to rapidly reversibly bind to TSP receptors, which reduces the likelihood of developing secondary resistance and reduces the risk of hypoglycemia. In therapeutic doses, this drug can reduce the severity of oxidative stress. These features of the pharmacokinetics of Diabeton MB allow its use in patients with heart disease, kidney disease and the elderly.

However, in each specific case, the dose of PSM should be selected individually, keeping in mind the high risk of hypoglycemic conditions in the elderly.

Gliquidone has two most characteristic features: short-term action and minimal excretion through the kidneys (5%). 95% of the drug is excreted from the body with bile. Effectively reduces fasting and postprandial blood glucose levels, and its short duration of action makes it easier to manage blood glucose levels and reduce the risk of hypoglycemia. Glurenorm is one of the safest sulfonylurea derivatives and the drug of choice in the treatment of elderly patients, patients with concomitant kidney diseases and people with predominant postprandial hyperglycemia.

Considering the clinical features of T2DM in old age, namely the predominant increase in postprandial glycemia, leading to high mortality from cardiovascular complications, in general, the prescription of TSP is especially justified in elderly patients.

Side effects may occur with the use of sulfonylurea drugs. This primarily concerns the development of hypoglycemia. In addition, there is a possibility of gastrointestinal disorders (nausea, vomiting, epigastric pain, less often - the appearance of jaundice, cholestasis), allergic or toxic reactions (skin itching, urticaria, Quincke's edema, leuko- and thrombocytopenia, agranulocytosis, hemolytic anemia, vasculitis). There is indirect evidence of the possible cardiotoxicity of PSM.

In some cases, during treatment with tableted glucose-lowering drugs, resistance to representatives of this group may be observed. In the case when the absence of the expected glucose-lowering effect is observed from the first days of treatment, despite changing drugs and increasing the daily dose to the maximum possible, we are talking about primary resistance to TSP. As a rule, its occurrence is due to a decrease in the residual secretion of its own insulin, which dictates the need to transfer the patient to insulin therapy.

Long-term use of TSP (more than 5 years) can cause a decrease in sensitivity to them (secondary resistance), which is due to a decrease in the binding of these drugs to receptors in insulin-sensitive tissues. In some of these patients, prescribing insulin therapy for a short period of time can restore the sensitivity of glucoreceptors and allow a return to the use of PSM.

Secondary resistance to tableted glucose-lowering drugs in general and to sulfonylurea drugs in particular can arise for a number of reasons: T1DM (autoimmune) is mistakenly diagnosed as type 2 diabetes mellitus, there is no use of non-pharmacological treatments for T2DM (diet therapy, dosed physical load), drugs with a hyperglycemic effect are used (glucocorticoids, estrogens, thiazide diuretics in large doses, l-thyroxine).

Exacerbation of concomitant or intercurrent diseases can also lead to a decrease in sensitivity to TSP. After relief of these conditions, the effectiveness of PSM can be restored. In some cases, with the development of true resistance to PSM, a positive effect is achieved through combination therapy with insulin and TSP or a combination of different groups of tableted glucose-lowering drugs.

Non-sulfonylurea secretagogues (glinides)

This is a new group of TSPs that stimulate the secretion of endogenous insulin, but do not belong to the group of sulfonylurea derivatives. Another name for these drugs is “prandial regulators”, which they received due to the extremely rapid onset and short duration of their action, which allows them to effectively regulate hyperglycemia after meals (postprandial hyperglycemia). The pharmacokinetics of these drugs necessitates their use immediately before or during meals, and the frequency of their intake is equal to the frequency of main meals (Table 11).

Table 11. Use of secretagogues

Indications for the use of secretagogues:

• newly diagnosed type 2 diabetes with signs of insufficient insulin secretion (without excess body weight);
• DM-2 with severe postprandial hyperglycemia;
• SD-2 in elderly and senile people;
• SD-2 with intolerance to other TSPs.

The best results with the use of these drugs were obtained in patients with a short history of T2DM, that is, with preserved insulin secretion. If the use of these drugs improves postprandial glycemia, and fasting glycemia remains elevated, they can be combined with metformin or long-acting insulin before bedtime.

Repaglinide is excreted from the body primarily through the gastrointestinal tract (90%) and only 10% in the urine, so the drug is not contraindicated in the early stages of renal failure. Nateglinide is metabolized in the liver and excreted in the urine (80%), therefore its use in persons with hepatic and renal insufficiency is undesirable.

The spectrum of side effects of secretagogues is similar to those for sulfonylurea drugs, since both stimulate the secretion of endogenous insulin.

Biguanides

Currently, of all the drugs in the biguanide group, only metformin (Glucophage, Siofor, Formin Pliva) is used. The glucose-lowering effect of metformin is due to several extrapancreatic mechanisms (that is, not related to insulin secretion by pancreatic B cells). Firstly, metformin reduces the increased production of glucose by the liver by suppressing gluconeogenesis, secondly, it increases the sensitivity to insulin of peripheral tissues (muscle and, to a lesser extent, fat), thirdly, metformin has a weak anorexigenic effect, fourthly, - slows down the absorption of carbohydrates in the intestine.

In patients with diabetes, metformin improves lipid metabolism by moderately reducing triglycerides (TG), low density lipoproteins (LDL), total cholesterol and LDL cholesterol in plasma. In addition, this drug has a fibrinolytic effect due to its ability to accelerate thrombolysis and reduce the concentration of fibrinogen in the blood.

The main indication for the use of metformin is type 2 diabetes with obesity and/or hyperlipidemia. In these patients, metformin is the drug of choice due to the fact that it helps reduce body weight and does not increase the hyperinsulinemia characteristic of obesity. Its single dose is 500-1000 mg, the daily dose is 2.5-3 g; the effective average daily dose for most patients does not exceed 2-2.25 g.

Treatment usually begins with 500-850 mg per day, if necessary increasing the dose by 500 mg at intervals of 1 week, taken 1-3 times a day. The advantage of metformin is its ability to suppress nocturnal hyperproduction of glucose by the liver. Taking this into account, it is better to start taking it once a day in the evening to prevent an increase in glycemia in the early morning hours.

Metformin can be used both as monotherapy with diet in people with type 2 diabetes and obesity, and in combination with PSM or insulin. This combination therapy is prescribed if the desired therapeutic effect is not achieved with monotherapy. Currently, there is a drug called glibomet, which is a combination of glibenclamide (2.5 mg/tab.) and metformin (400 mg/tab.).

The most serious potential complication of biguanide therapy is lactic acidosis. A possible increase in lactate levels in this case is associated, firstly, with the stimulation of its production in the muscles, and secondly, with the fact that lactate and alanine are the main substrates of gluconeogenesis suppressed when taking metformin. However, it should be assumed that metformin, prescribed according to indications and taking into account contraindications, does not cause lactic acidosis.

Taking into account the pharmacokinetics of metformin, its temporary withdrawal is necessary when administering radiopaque iodine-containing substances, before the upcoming general anesthesia (at least 72 hours), in the perioperative period (before surgery and several days after it), with the addition of acute infectious diseases and exacerbation of chronic ones.

Metformin is generally well tolerated. Side effects, if they develop, occur at the very beginning of treatment and quickly disappear. These include: flatulence, nausea, diarrhea, discomfort in the epigastric region, decreased appetite and a metallic taste in the mouth. Dyspeptic symptoms are mainly associated with slower absorption of glucose in the intestine and increased fermentation processes.

In rare cases, intestinal absorption of vitamin B12 is impaired. An allergic reaction may occur. Due to the lack of a stimulating effect on insulin secretion, metformin extremely rarely causes the development of hypoglycemia, even with an overdose and skipping meals.

Contraindications to the use of metformin are: hypoxic conditions and acidosis of any etiology, heart failure, severe dysfunction of the liver, kidneys, lungs, old age, alcohol abuse.

When treating with metformin, monitoring of a number of indicators is necessary: hemoglobin (once every 6 months), the level of creatinine and serum transaminases (once a year), and, if possible, the level of lactate in the blood (once every 6 months). If muscle pain occurs, an emergency blood lactate test is necessary; Normally its level is 1.3-3 mmol/l.

Thiazolidinediones (glitazones) or sensitizers

Thiazolidinediones are new tableted glucose-lowering drugs. The mechanism of their action is the ability to eliminate insulin resistance, which is one of the main causes of the development of T2DM. An additional advantage of thiazolidinediones over all other TSPs is their lipid-lowering effect. The greatest hypolipidemic effect is exerted by actos (pioglitazone), which can eliminate hypertriglyceridemia and increase the content of antiatherogenic high density lipoproteins (HDL).

The use of thiazolidinediones in patients with type 2 diabetes opens up prospects for the prevention of cardiovascular complications, the development mechanism of which is largely due to existing insulin resistance and lipid metabolism disorders. In other words, these drugs increase the sensitivity of peripheral tissues to the physiological action of their own endogenous insulin and at the same time reduce its concentration in the blood.

In the absence of secretion of endogenous insulin (DM-1) or in the case of a decrease in its secretion (prolonged course of type 2 diabetes mellitus, accompanied by unsatisfactory compensation at the maximum dose of TSP), these drugs cannot have a hypoglycemic effect.

Currently, two drugs from this group are used: rosiglitazone (Avandia) and pioglitazone (Actos) (Table 12).

Table 12. Use of thiazolidinediones

80% of drugs in this group are metabolized by the liver and only 20% are excreted by the kidneys.

Thiazolidinediones do not stimulate insulin secretion by the pancreas, therefore they do not cause hypoglycemic conditions and help reduce fasting hyperglycemia.

During treatment with glitazones, mandatory monitoring of liver function (serum transaminases) is required once a year. Other possible side effects may include swelling and weight gain.

Indications for the use of glitazones are:

• newly diagnosed T2DM with signs of insulin resistance (with only diet therapy and physical activity ineffective);
• SD-2 with ineffectiveness of average therapeutic doses of PSM or biguanides;
• CD-2 with intolerance to other glucose-lowering drugs.

Contraindications for the use of glitazones are: increase in the level of serum transaminases by more than 2 times, heart failure of the III-IV degree.

Drugs of this class can be used in combination with sulfonylureas, metformin and insulin.

α-glucosidase inhibitors

This group of drugs includes drugs that inhibit gastrointestinal enzymes involved in the breakdown and absorption of carbohydrates in the small intestine. Undigested carbohydrates enter the large intestine, where they are broken down by intestinal flora into CO 2 and water. At the same time, the ability of glucose resorption and entry into the liver decreases. Preventing rapid intestinal uptake and improving hepatic glucose utilization results in decreased postprandial hyperglycemia, decreased pancreatic B cell load, and decreased hyperinsulinemia.

Currently, the only drug from this group is registered - acarbose (Glucobay). Its use is effective at high levels of glycemia after meals and at normal levels on an empty stomach. The main indication for the use of glucobaya is mild type 2 diabetes mellitus. Treatment begins with a small dose (50 mg with dinner), gradually increasing it to 100 mg 3 times a day (optimal dose).

With glucobay monotherapy, hypoglycemic reactions do not develop. The possibility of using the drug in combination with other tableted glucose-lowering drugs, especially those stimulating insulin secretion, may provoke the development of a hypoglycemic reaction.

Side effects of acarbose include flatulence, bloating, diarrhea; an allergic reaction is possible. With continued treatment and diet (excluding excess carbohydrate consumption), gastrointestinal complaints disappear.

Contraindications to the use of acarbose:

• intestinal diseases accompanied by malabsorption;
• the presence of diverticula, ulcers, stenoses, fissures of the gastrointestinal tract;
• gastrocardial syndrome;
• hypersensitivity to acarbose.

T.I. Rodionova

Catad_tema Diabetes mellitus type II - articles

Modern tactics for treating type 2 diabetes mellitus

M.I.Balabolkin, V.M.Kreminskaya, E.M.Klebanova
Department of Endocrinology and Diabetology FPPO MMA named after I.M. Sechenov, Moscow

Diabetes mellitus (DM) type 2 is a heterogeneous disease, the development of which is caused by the presence of insulin resistance and impaired insulin secretion by b-cells of the pancreatic islets. It becomes clear that therapy for type 2 diabetes cannot be as unified as it is for type 1 diabetes.

The goal of treatment for type 2 diabetes is to achieve diabetes compensation over a long period of time, i.e. indicators of glucose in the blood plasma, which are almost identical to those observed in a healthy person throughout the day. However, qualitative and quantitative indicators of diabetes compensation have been repeatedly revised based on ongoing studies establishing the dependence of the development of late vascular complications of diabetes on the state of carbohydrate metabolism. The dynamics of quantitative indicators of diabetes compensation are presented in Table. 1.

Currently, no one doubts that strict and long-term compensation of carbohydrate metabolism reduces the incidence of complications of diabetes. This is convincingly shown by the results of the DCCT (1993) and UKPDS (1998) studies. Maintaining glycemia close to normal values ​​during the observation period (about 10 years) made it possible to achieve primary prevention of retinopathy in patients with type 1 diabetes by 76%; secondary prevention of retinopathy - by 54%; prevention of neuropathy - by 60%; achieve the disappearance of microalbuminuria - by 39% and albuminuria - by 54%. The same effects can be achieved in type 2 diabetes, since the mechanisms underlying the development of complications are probably the same. Thus, it was found that intensive glucose-lowering therapy reduces the risk of myocardial infarction by 16%. Therefore, as before, the main task of treating diabetes is to achieve its compensation over a long period of time, which is fraught with great difficulties. This is mainly due to the fact that treatment for diabetes is usually prescribed not from the moment of disturbance of carbohydrate metabolism, which is detected only through various stress tests (glucose tolerance test, etc.), but only when pronounced clinical signs of diabetes appear, which in turn indicate the development vascular and other changes in tissues and organs.

Table 2.
Compensation criteria for type 2 diabetes mellitus

Indicators	Low risk	Risk of arterial damage	Risk of microangiopathy
Venous blood plasma Fasting/before meals
Capillary blood glucose (self-monitoring)
On an empty stomach/before meals
Postprandial glucose (peak)

Table 3.
Criteria for the state of lipid metabolism in patients with type 2 diabetes mellitus

Thus, an analysis of the clinical manifestations of diabetes detected during its manifestation in adults shows a high frequency of late vascular complications, the development of which occurs when carbohydrate metabolism disorders last for 5-7 years. Our study of the frequency of vascular complications in type 2 diabetes shows that 44% of patients with newly diagnosed diabetes have one or two (retinopathy, nephropathy, macroangiopathy, etc.) vascular complications of diabetes.

The main role in the pathogenesis of vascular complications of diabetes belongs to hyperglycemia, and in type 2 diabetes, lipid metabolism disorders. European Bureau of the International Federation of Diabetes and WHO European Bureau in 1998. proposed criteria for metabolic compensation in patients with type 2 diabetes, which are presented in Table. 2.

In type 2 diabetes, disturbances in carbohydrate metabolism are combined with pronounced changes in lipid metabolism. In this regard, when considering the compensation of metabolic processes, one should also take into account indicators of the state of lipid metabolism, which to one degree or another correlate with the risk of developing vascular complications of diabetes (Table 3).

The adequacy of diabetes therapy remains the most pressing issue, since it has been established that hyperglycemia is the trigger for many pathogenetic mechanisms that contribute to the development of vascular complications.

Strict compensation for diabetes, i.e. By maintaining normal (or close to normal) blood glucose concentrations for a long time, it is possible to delay or delay the onset of late complications of diabetes.

Treatment of type 2 diabetes

Treatment of type 2 diabetes is complex, and its components are: diet; dosed physical activity; patient education and diabetes self-management; drug therapy (oral hypoglycemic drugs as monotherapy, combination therapy with oral drugs - drugs with different mechanisms of action, combination therapy of oral hypoglycemic drugs with insulin, or the use of insulin therapy alone); prevention and treatment of late complications of diabetes.

Diet for type 2 diabetes, it must meet the following requirements: a) be physiological in the composition of the products (about 60% of the total caloric content of food should be carbohydrates, 24% - fats and 16% - proteins); b) the energy value of food should be subcaloric (daily calorie content is about 1600-1800 kcal); c) 4-5 meals a day; d) exclude easily digestible carbohydrates from the diet and replace them with sweeteners or sugar substitutes; e) food must contain a sufficient amount of fiber or fiber (at least 25-30 g per day); e) of the total amount of fat, about 40-50% should be fats of vegetable origin (1/3 of the total amount of fat should be saturated fats; 1/3 - semi-unsaturated and 1/3 - unsaturated fats).

Multiple (4-5 times) meals during the day allow you to more adequately modulate the relationship between the level of insulin and glucose in the blood, approaching those indicators that occur in a healthy person throughout the day.

Physical activity and physical therapy are a mandatory component of therapy for patients with type 2 diabetes. The amount of physical activity should be determined taking into account the patient’s age, the state of the cardiovascular system and compensation of carbohydrate metabolism. They have a positive effect on the course of diabetes and help maintain stable compensation of carbohydrate metabolism with a noticeable decrease in excess body weight. Regular physical exercise, regardless of its volume, helps normalize lipid metabolism, improves microcirculation, activates fibrinolysis, normalizes increased secretion of catecholamines in response to a stressful situation, which ultimately prevents the development of vascular complications (angiopathy). In diabetic patients who regularly engage in physical exercise, stabilization and even regression of vascular complications of diabetes are noted.

The task patient education Type 2 diabetes is their motivation to change lifestyle and habits that accompanied the patient throughout his life before developing diabetes. This applies primarily to diet (almost 50% of the daily calorie intake occurs in the second half of the day or dinner), sleep and rest patterns, reducing physical inactivity through regular physical activity, quitting smoking and taking excessive doses of alcohol, and doing all those activities that are components of a healthy lifestyle. Self-control of diabetes and achieving its compensation will help delay the development of vascular complications of diabetes.

Drug therapy

Drug therapy for patients with type 2 diabetes includes: a) the use of various medications that reduce the absorption of carbohydrates in the gastrointestinal tract (acarbose, etc.); b) biguanides (metformin); c) glitazones or insulin sensitizers (pioglitazone); d) the use of drugs that stimulate insulin secretion: sulfonylurea drugs of the second generation: glibenclamide, glipizide, gliclazide, gliquidone and sulfonylurea drugs of the third generation (glimepiride), as well as drugs derived from amino acids, repaglinide and nateglinide, which are regulators of postprandial hyperglycemia or stimulants of secretion short-acting insulin. In cases where it is not possible to achieve compensation for diabetes with the help of oral hypoglycemic drugs (in patients with type 2 diabetes with a pronounced defect of b-cells of the pancreatic islets), it is recommended to use combination therapy (oral glucose-lowering therapy + insulin therapy, more often with drugs of medium duration of action on night or 2 times a day).

Sulfonylureas represent the main group of drugs used to treat type 2 diabetes. These drugs are insulin secretogens, and their main hypoglycemic effect is associated with stimulation of the formation and release of insulin from the pancreatic islets. In recent years, the mechanism of action of sulfonylurea drugs on stimulating insulin secretion by pancreatic b-cells has been completely deciphered. These drugs bind to the corresponding receptors localized on the membranes of b-cells, change the activity of K-ATPase, promote the closure of potassium channels (KATP-dependent channels) and increase the ratio of ATP/ADP levels in the cytoplasm, which leads to membrane depolarization. This, in turn, promotes the opening of voltage-dependent Ca2+ channels, increasing the level of cytosolic calcium and stimulating Ca2+-dependent exocytosis of secretory granules, which results in the release of the contents of the secretory granule into the intercellular fluid and blood. The last step of insulin secretion is under the control of calcium/calmodulin-dependent protein kinase II. Thus, the target of action of sulfonylurea drugs is ATP-sensitive potassium channels, which consist of the sulfonylurea receptor [140-kDa protein (SUR)] and a specific protein (KIR6.2).

However, all 2nd generation sulfonylurea derivatives have certain disadvantages of greater or lesser severity, which do not allow in all cases to achieve stable compensation for diabetes and normalization of carbohydrate metabolism parameters both over a long period of time and throughout the day. The latter is due to the fact that the peak effect of any sulfonylurea drug and the increase in post-absorption hyperglycemia do not coincide in time. This leads, on the one hand, to an insufficient decrease in blood glucose levels for a long time, and on the other, to the development of hypoglycemia of varying severity in the hours following a meal, especially in the case of insufficient food or skipping a meal. Episodes of hypoglycemia are more common in elderly patients as a result of a violation of the regimen of using glucose-lowering drugs due to memory impairment. For example, when taking glibenclamide 2-3 times, patients often forget whether they took the drug in the morning. To compensate for the possible absence of taking the drug before breakfast, the patient takes a double dose before dinner, which leads to the development of hypoglycemia at night.

The study of the molecular mechanisms of action of sulfonylurea drugs made it possible to obtain data that shed light on the interaction processes of various stimulants of insulin secretion and showed that insulin secretogens, despite the identical final effect, manifested in increased secretion and release of insulin from b-cells, carry out this effect through involvement in corresponding process of various protein and signaling molecules.

ATP-sensitive potassium channels are the primary structures that interact with various insulin secretogens. ATP-sensitive potassium channels are a complex that includes sulfonylurea receptor 1 [molecular weight protein 140,000 (SUR1) and a specific protein, the so-called internal potassium channel scavenger or rectifying subunit KIR6.2. The gene encoding the SUR1 receptor is localized on chromosome 11p15.1 and belongs to the family of ATP-binding cassette proteins (ABC proteins), which has 17 transmembrane domains (TMDs), in which there are two nucleotide-binding regions - NBF-1 and NBF-2, specifically complexing with Mg2+ ADP/ATP. ATP-sensitive channels are like two proteins - SUR1 and KIR6.2, which are coexpressed together. The KIR6.2 locus is located inside the SUR1 gene, i.e. on the same 11p15.1 chromosome.

Thus, ATP-sensitive potassium channels are assembled from two different subunits: the sulfonylurea receptor, which belongs to the ATP-binding cassette family, and the potassium channel subunits (KIR6x), forming a pore and a regulatory subunit. Three isoforms of the sulfonylurea receptor have been cloned: SUR1 - high-affinity receptor and SUR2, SUR2B - low-affinity receptors. Structurally, potassium channels in different tissues are different in their constituent subunits. Thus, in b-cells of the pancreatic islets and glucose-sensitive neurons of the hypothalamus, they consist of SUR1/KIR6.2; in cardiac muscle - from SUR2A/KIR6.2 and in vascular smooth muscle cells - from SUR2B/KIR6.1 (or KIR6.2). It was shown that the ability of various drugs (glibenclamide, glipizide, tolbutamide and meglitinide) to inhibit potassium channels (SUR1/KIR6.2 and SUR2B/KIR6.2) was 3-6 times higher than their affinity for complexing with these receptors. Closure of the potassium channel requires binding of one of the four sulfonylurea binding sites on the “channel complex,” which is represented by the octometric structure (SUR/KIR6x)4.

The key to understanding the mechanism of action of various sulfonylurea drugs was studies in which it was shown that the latter complex with certain areas of the TMD. Thus, glibenclamide complexes with the 1-5 TMD region, and tolbutamide with 12-17 TMD, which indicates a modular structural and functional organization of ATP-sensitive potassium channels. Glibenclamide, as a result of conformational changes, disrupts the interaction between NBF 1 and 2 of SUR1 at TMD 12-17 and especially TMD 1-5. This in turn causes the translocation of the TMD2KIR6.2 complex, which is in direct contact with TMD 1-5 SUR1, to induce a “gated potassium channel” state. This mechanism requires the amino-terminal end of KIR6.2 to be intact. Thus, sulfonylurea binding to SUR1 clearly causes an underlying reduction in the required binding strength between SUR1 and KIR6.2, which is required to maintain KIR6.2 at least partially in the open state.

The opening and closing of ATP-sensitive potassium channels, and consequently the initiation and inhibition of insulin secretion, is ensured by the complexation of ATP with various subunits of potassium channels. ATP binding to the carboxy-terminal domain of KIR6.2 stabilizes glibenclamide-induced dissociation of SUR1 and KIR6.2 and promotes potassium channel closure. Complexation of ATP with NBF-1 and Mg2+ ADP with NBF-2 on SUR1 causes the opening of potassium channels.

Despite the fact that glibenclamide and glimepiride have a stimulating effect on insulin secretion by closing ATP-sensitive potassium channels, the mechanism of this effect has certain differences. It has been established that glimepiride has an association rate constant that is 2.2-3 times higher, and a dissociation rate that is 8-10 times higher than that of glibenclamide. These data indicate that the affinity of glimepiride for the sulfonylurea receptor is 2-3 times lower than that of glibenclamide. In addition, glibenclamide complexes with a receptor polypeptide having a molecular weight of 140 kDa, while glimepiride complexes with a polypeptide of the same receptor, but having a molecular weight of 65 kDa, which is designated SURX. Additional studies have shown that glibenclamide, in addition to the main complexation with the 140 kDa polypeptide, also specifically complexes with proteins with a molecular weight of 40 and 65 kDa, which made it possible to suggest that glibenclamide can also complex with the SURX protein, although the affinity for such complexation it is significantly lower than that of glimepiride. All of the above suggests that the target proteins of the sulfonylurea receptor for glibenclamide and glimepiride are different: for glibenclamide - SUR1, for glimepiride - SURX. Both proteins interact with each other and control, through KIR6.2, the opening and closing of potassium channels, and therefore the processes of insulin synthesis and release in the pancreatic b-cell.

Since the use of sulfonylureas for the treatment of type 2 diabetes, discussions about the extrapancreatic (peripheral) action of sulfonylureas have continued. The laboratory, led by G. Muller, has been conducting research in this direction for many years. Studying in vitro and in vivo the effect of glimepiride, glipizide, glibenclamide and gliclazide on the maximum decrease in blood glucose levels and the minimum increase in insulin secretion within 36 hours after taking these drugs, it was found that glimepiride at a dose of 90 μg/kg caused a maximum decrease in glucose levels in the blood with minimal insulin secretion; glipizide at a dose of 180 μg/kg had the lowest hypoglycemic activity and caused the maximum increase in insulin secretion; Glibenclamide at a dose of 90 μg/kg and gliclazide at a dose of 1.8 mg/kg occupied an intermediate position between the two extremes. The curves for the dynamics of the concentrations of insulin and glucose in the blood when using these sulfonylurea drugs were almost identical. However, when determining the coefficient (the average increase in plasma insulin levels to the average decrease in blood glucose), these indicators turned out to be unequal (glimepiride - 0.03; gliclazide - 0.07; glipizide - 0.11 and glibenclamide - 0.16). This difference was a consequence of lower insulin secretion: for glimepiride, the average plasma insulin level was 0.6 μU/ml, for gliclazide - 1.3; for glipizide - 1.6 and glibenclamide - 3.3 µU/ml (G. Muller, 2000). The least stimulating effect of glimepiride on insulin secretion provides a lower risk of developing hypoglycemia.

The results of these studies indicate that sulfonylureas have some degree of peripheral effect, but this effect is more pronounced with glimepiride. The peripheral effect of glimepiride is due to the activation of GLUT-4 translocation (to a lesser extent GLUT-2) and an increase in the synthesis of fat and glycogen in adipose and muscle tissues, respectively. In the plasma membrane of adipocytes under the influence of glimepiride, the amount of GLUT-4 is 3-3.5 times higher, and insulin is 7-8 times higher. In addition, glimepiride causes dephosphorylation of GLUT-4, which is an obligatory condition for stimulating key enzymes of lipogenesis (glycerol-3-phosphate acyltransferase) and glycogenesis (glycogen synthetase). Glimepiride, like glibenclamide, increases the coefficient of glycogen synthetase activity to 45-50% of the maximum effect of insulin. At the same time, the activity of glycerol-3-phosphate acyltransferase increases to 35-40% of the maximum effect of insulin. Glimepiride inhibits the activity of protein kinase A and lipolysis through activation of cAMP-specific phosphodiesterase.

The most effective drug from the group of sulfonylurea drugs is glibenclamide, which was introduced into clinical practice in 1969. The biological half-life is 5 hours, and the duration of the hypoglycemic effect is up to 24 hours. The drug is metabolized mainly in the liver by conversion into two inactive metabolites, one of which is excreted in the urine, and the second is excreted through the gastrointestinal tract. The daily dose is 1.25-20 mg (maximum daily dose - 20-25 mg), which is prescribed in 2, less often in 3 doses, 30-60 minutes before meals. Glibenclamide has the most pronounced hypoglycemic effect among the entire group of sulfonylurea drugs, and in this regard it is rightfully considered the “gold standard”. On the domestic market, glibenclamide is presented in tablets of 5; 3.5; and 1.75 mg. Moreover, the last two dosage forms are micronized, which makes it possible to maintain its therapeutic concentration in the blood at a lower dose of the drug, i.e. With a smaller dose of the drug, it is possible to achieve a higher effectiveness of its action. If the bioavailability of glibenclamide in 5 mg tablets is 29-69%, then its micronized forms are 100%. Glibenclamide (5 mg) is recommended to be taken 30-40 minutes before meals, and its micronized forms - 7-8 minutes. The maximum effect of micronized glibenclamide almost completely coincides with post-absorption hyperglycemia, therefore, in patients receiving micronized forms of the drug, hypoglycemic conditions are observed much less frequently, and if they develop, they occur in a mild form.

Glipizide has been used for the treatment of type 2 diabetes since 1971 and is almost equal in its hypoglycemic effect to glibenclamide. It is quickly and completely absorbed from the gastrointestinal tract. The biological half-life in plasma is 2-4 hours, the hypoglycemic effect lasts 6-12 hours, and its retard form has a duration of action of 24 hours.

At the same time, dosage forms of well-known drugs (gliclazide and glipizide) with a prolonged effect were obtained. Prolongation of the action of these drugs is due to the use of technologies that slow down the absorption of the drug from the intestine.

Gliclazide proposed as a hypoglycemic drug in 1970. Gliclazide is also a second generation drug, its daily dose is 30–120 mg (available in 30 mg tablets). Our studies have shown that when treated with gliclazide, patients experienced a significant decrease in platelet aggregation, a significant increase in the relative disaggregation index, an increase in heparin and fibrinolytic activity, and an increase in heparin tolerance, which suggested a normalizing effect of gliclazide on the functional state of blood platelets. There was a significant tendency towards an improvement in the aggregation function of erythrocytes, as well as a decrease in blood viscosity at low shear stresses. Plasma-coagulation factors of blood coagulation, fibrinolysis, indicators of protein and lipid metabolism also tended to normalize. It stabilizes the course of microangiopathy and even causes reverse development in some cases.

Gliquidone is also a sulfonylurea derivative, and is also classified as a second generation drug. However, like gliclazide, in terms of its characteristics it does not fully possess all the characteristics required for this group. The drug is available in 30 mg tablets, and the daily dose is 30-120 mg. The difference between gliquidone and drugs in this group is that 95% of the drug taken orally is excreted through the gastrointestinal tract and only 5% through the kidneys, while almost 100% of chlorpropamide and 50% of glibenclamide are excreted in the urine. The hypoglycemic effect of gliquidone is weaker compared to the listed drugs.

In addition, to the great satisfaction of endocrinologists, glimepiride was proposed for the treatment of type 2 diabetes in the second half of the 90s. This is the first sulfonylurea drug with a prolonged action and a low therapeutic dose (1-4 mg per day) compared to other sulfonylurea drugs. These differences made it possible to classify glimepiride as a third generation of sulfonylurea drugs.

Glimepiride is the first sulfonylurea drug with a prolonged action and a low therapeutic dose (1-4 mg per day) compared to other sulfonylurea drugs. These differences made it possible to classify it as a third generation (generation) of sulfonylurea drugs. The half-life of glimepiride is longer (more than 5 hours) than other drugs in this group, which ensures its therapeutic effectiveness within 24 hours. The drug is prescribed once a day in a dose of 1–4 mg, the maximum recommended dose is 6 mg. Glimepiride is completely metabolized in the liver to metabolically inactive products.

For many years, various pharmaceutical companies have been conducting research to find new oral glucose-lowering drugs. One of these developments is the synthesis of a new oral hypoglycemic substance - repaglinide , which is a derivative of benzoic acid. Repaglinide is structurally related to meglitinide, which has a non-sulfourea specific part of the glibenclamide molecule and, like sulfonylurea drugs, stimulates insulin secretion by the mechanism described for sulfonylurea drugs.

Biguanides. The second group of oral hypoglycemic drugs includes biguanides, which are represented by phenethyl biguanide (phenformin), N,N-dimethyl biguanide (metformin) and L-butyl biguanide (buformin).

The difference in the chemical structure of these drugs has little effect on their pharmacodynamic effect, causing only a slight difference in the manifestation of the hypoglycemic activity of each of them. However metformin is not metabolized in the body and is excreted unchanged by the kidneys, while phenformin is only 50% excreted unchanged, and the rest is metabolized in the liver. These drugs do not change insulin secretion and have no effect in its absence. Biguanides increase the peripheral utilization of glucose in the presence of insulin, reduce gluconeogenesis, and increase the utilization of glucose by the intestine, which is manifested by a decrease in the level of glucose in the blood flowing from the intestine; and also reduce the elevated levels of insulin in the blood serum in patients suffering from obesity and type 2 diabetes. Their long-term use has a positive effect on lipid metabolism (lowering cholesterol and triglycerides). Biguanides increase the amount of GLUT-4, which manifests itself in improved glucose transport across the cell membrane. It is this effect that explains their potentiating effect on the action of insulin. The site of action of biguanides is probably also the mitochondrial membrane. By inhibiting gluconeogenesis, biguanides contribute to an increase in the content of lactate, pyruvate, alanine, i.e. substances that are precursors of glucose in the process of gluconeogenesis. Due to the fact that under the action of biguanides the amount of increasing lactate exceeds the formation of pyruvate, this may be the basis for the development of lactic acidosis (lactic acidosis).

In Russia, as in all countries of the world, only metformin is used from the biguanide group. The half-life of metformin is 1.5-3 hours. The drug is available in tablets of 0.5 and 0.85 g. Therapeutic doses are 1-2 g per day (maximum up to 2.55-3 g per day).

The hypoglycemic effect of metformin is due to several mechanisms. A decrease in the level of glucose in the blood flowing from the liver indicates a decrease in both the rate and the total amount of glucose produced by the liver, which is a consequence of inhibition of gluconeogenesis through inhibition of lipid oxidation. Under the influence of metformin, glucose utilization in the periphery increases due to the activation of post-receptor mechanisms of action of insulin and in particular tyrosine kinase and phosphotyrosine phosphatase. In addition, the peripheral effects of metformin are mediated by its specific effect on the synthesis and pool of glucose transporters in the cell. . The utilization of glucose by the intestinal mucosa increases. The number of glucose transporters (GLUT-1, GLUT-3 and GLUT-4) increases under the influence of metformin in the plasma membrane of both adipocytes and monocytes. Glucose transport increases in the endothelium and vascular smooth muscle, as well as in the heart muscle. It is this effect that explains the decrease in insulin resistance in patients with type 2 diabetes under the influence of metformin. An increase in insulin sensitivity is not accompanied by an increase in its secretion by the pancreas. At the same time, against the background of a decrease in insulin resistance, the basal level of insulin in the blood serum decreases. Patients treated with metformin experience weight loss, in contrast to what may occur with overdose of sulfonylureas and insulin. Moreover, body weight loss occurs mainly due to a decrease in adipose tissue. In addition, metformin helps reduce serum lipids. At the same time, the concentration of total cholesterol, triglycerides, low and very low density lipoproteins decreases and, possibly, the level of high density lipoproteins increases, which has a positive effect on the course of macroangiopathy.

In recent years, it has been established that under the influence of metformin, fibrinolysis increases, which is reduced in patients with type 2 diabetes and is an additional factor in thrombus formation and vascular complications of diabetes. The main mechanism of action of metformin to increase fibrinolysis is a decrease in the level of plasminogen activator inhibitor-1, which occurs in patients with type 2 diabetes, regardless of its dose. In addition to reducing the activity of plasminogen activator inhibitor-1, metformin also reduces the proliferation of smooth muscle cells in the vascular wall in vitro and the rate of atherogenesis in animals.

Metformin does not reduce blood glucose levels below its normal level, which is why there are no hypoglycemic conditions when treating patients with diabetes with this drug.

It was noted above that sulfonylurea drugs stimulate insulin secretion, and metformin promotes the utilization of glucose by peripheral tissues, i.e. drugs, acting on various mechanisms, contribute to better compensation of diabetes. Combination therapy with sulfonylureas and metformin has been used for a long time and with good effect. Therefore, some companies have already mastered the production of combined action drugs.

Alpha-glucosidase inhibitors (acarbose)- this is the third group of oral hypoglycemic drugs, which have been widely used for the treatment of diabetes in the last 8-10 years in order to reduce the absorption of carbohydrates from the intestine and the main effect of which is associated with inhibition of the activity of enzymes involved in the digestion of carbohydrates. It is known that food carbohydrates, more than 60% of which are starch, are first hydrolyzed in the gastrointestinal tract by specific enzymes (glycosidases: beta-glucuronidase, beta-glucosaminidase, alpha-glucosidase, etc.) and then break down into monosaccharides. The latter are absorbed through the intestinal mucosa and enter the central circulation. Recently, it has been shown that in addition to the main effect of glucosidase inhibition, alpha-glucosidase inhibitors improve peripheral glucose utilization by increasing the expression of the GLUT-4 gene. The drug is well tolerated by patients and can be used to treat patients with type 2 diabetes in cases where it is not possible to achieve compensation for carbohydrate metabolism only on diet and adequate physical activity.

Usual doses of acarbose range from 50 mg per day, gradually increasing to 50 mg 3 times a day and then to 100 mg 3 times a day. In this case, it is possible to avoid such undesirable phenomena as discomfort in the gastrointestinal tract, flatulence, and loose stools. The drug must be taken with the first sip of food (i.e. during meals). There is no hypoglycemia with acarbose monotherapy.

Potentiators (or sensitizers) of insulin action increase the sensitivity of peripheral tissues to insulin. Drugs in this group include glitazones or thiazolidinediones - pioglitazone and rosigditazone.

Treatment algorithm for type 2 diabetes

Thus, the modern treatment algorithm for type 2 diabetes includes: diet therapy, lifestyle changes (regular physical activity, smoking cessation, patient education), and if there is no effect, additional use of acarbose. If obesity is present, anorectics may be recommended. In case of insufficient effect from taking acarbose with excess body weight (ideal body weight 30 kg/m2 or more), combined treatment with metformin or sulfonylurea drugs (with ideal body weight up to 30 kg/m2). In these cases, a combination of metformin with sulfourea drugs is possible (in case of excess weight). Insulin sensitizers (pioglitazone, usually 30 mg once daily) can be used as monotherapy or in combination with sulfonylureas and metformin. All of the listed oral hypoglycemic drugs can be used as monotherapy or in combination.

If the effect of the treatment is unsatisfactory, insulin therapy is indicated in the future. The criteria for prescribing insulin therapy for type 2 diabetes are: lack of compensation for diabetes when using diet therapy in combination with glucosidase inhibitors, biguanides, insulin sensitizers or insulin secretogens (sulfonylureas and drugs derived from amino acids) and so-called secondary insulin resistance to oral drugs.

According to various authors, secondary resistance to sulfonylureas occurs in 5-20% of patients with diabetes and is associated with a decrease in residual insulin secretion. Secondary resistance to oral drugs is detected in 4.1% of patients 1 year from the onset of the disease, and in 11.4% after 3 years.

The study of the pathogenesis of secondary resistance to oral drugs has made it possible to establish its various mechanisms. In some patients, secondary resistance to oral hypoglycemic drugs occurs with reduced residual secretion of insulin and C-peptide, while antibodies to cellular antigens of the pancreatic islets are absent. Based on the characteristics of the clinical course of the disease, these patients can be divided into 2 groups: 1) patients with type 2 diabetes with temporary insulin requirements; 2) patients with a constant need for insulin or even insulin dependence (LADA subtype).

The first group consists of patients with diabetes for 10 years or more and those who are overweight. To compensate for carbohydrate metabolism, two therapeutic tactics are recommended in these cases. The first is the complete transfer of patients to insulin therapy for a short time (2.5-4 months). This time is sufficient to relieve glucotoxicity and lipotoxicity, restoring the sensitivity of beta cells to sulfonylureas and restoring the reserve capacity of the pancreatic islets. A prerequisite for relieving glucotoxicity is achieving full compensation of diabetes during the period of insulin therapy. Subsequently, patients are again transferred to oral therapy with good or satisfactory compensation results.

The second tactic is to carry out combination therapy with insulin and oral hypoglycemic drugs. For the treatment of patients with type 2 diabetes with secondary resistance to oral drugs, we have been using both treatment tactics for 10-12 years. We used combination therapy with insulin in a daily dose, usually no more than 30 units. per day (usually intermediate-acting insulin). It is more advisable to prescribe insulin at night, i.e. at 22 or 23 o'clock. The onset of action of such an insulin preparation occurs in the morning hours or during the period when there is excessive production of glucose by the liver. The result of this is a significant decrease in fasting blood glucose. In some cases, it is necessary to administer these insulin preparations twice (in the morning and at 10-11 p.m.). During the day, to maintain the hypoglycemic effect, it is recommended to take sulfonylurea drugs (glimepiride at a dose of 2-3 mg per day, glibenclamide at a dose of 10-15 mg per day or gliclazide at a dose of 60-180 mg per day). It is recommended to start insulin therapy with 10-12 units. and increase by 2-4. every 3-4 days until fasting glucose decreases to 5-6.8 mmol/l. Determination of glycemia during the day is necessary at least once a week during the period of selection of doses of glucose-lowering drugs (insulin and oral drugs). In addition to determining fasting glucose, it is extremely necessary to have data on blood glucose levels before lunch and dinner, as well as 1 hour after meals.

In cases where patients require insulin therapy, the latter can be carried out in a multiple injection regimen or, more often, in a double injection regimen. In the latter case, we obtained good results using combined action insulin preparations. Combined-action insulin preparations are administered before breakfast and before dinner.

In addition, the double injection regimen can be used when using short- and medium-acting insulin preparations. In this case, it is necessary to use short- and medium-acting insulin before breakfast, a short-acting insulin before dinner, and a medium-acting insulin before bedtime (at 10 or 11 p.m.). The ratio of short-acting insulin to intermediate-acting insulin in the morning is 1:3 (25% and 75%), and in the evening – 1:2 or even 1:1. The regimen of multiple injections of insulin, which is necessary to control type 1 diabetes, was also used to treat patients with type 2 diabetes. In these cases, both intermediate-acting insulins and long-acting insulin preparations can be used as basal-acting insulin. However, there is practically no advantage of the multiple injection regimen over the double insulin administration regimen.

As for the dose of insulin, to compensate for type 2 diabetes, a daily dose of 0.6-0.8 units per 1 kg of body weight is required. In some cases, the dose of the drug has to be increased to 0.9-1.0 units per 1 kg or even more. This is explained by insulin resistance, which is so characteristic of type 2 diabetes. When diabetes compensation is achieved, in such cases the insulin requirement decreases and the doses of insulin required to maintain diabetes compensation are correspondingly reduced.

Achieving compensation for type 2 diabetes mellitus is a prerequisite for the prevention of vascular complications, early disability and increased mortality in this disease.

Type 2 diabetes mellitus is a chronic pathology that predominantly develops in people with abdominal obesity. This is an insidious disease, which does not manifest itself in any way at the initial stages, but later without treatment can lead to catastrophic complications that can lead to a person’s disability and even lead to death. This pathology cannot be completely cured, but treatment of type 2 diabetes mellitus is extremely necessary in order to learn how to manage the disease.

Treatment methods:

1. Lifestyle correction (diet therapy, physical activity, influence on stress factors).
2. Drug therapy (sugar-lowering tablets, insulin injections).

Despite the fact that there are a sufficient number of hypoglycemic drugs in different forms, it is impossible to reduce the impact of lifestyle changes as one of the areas of treatment for type 2 diabetes. Let's take a closer look at how exactly factors predisposing to diabetes need to be corrected.

• swimming;
• walking at a moderate pace;
• a ride on the bicycle;
• light morning exercises, etc.

It is important to understand that the main thing is not the intensity of the load, but its regularity. Correcting diabetes does not require exhausting training, but a sedentary lifestyle will not help the disease, so together with your endocrinologist you need to choose your pace, the duration of the load, taking into account all additional factors: age, individual exercise tolerance and the presence of concomitant pathology.

Positive effects of physical activity:

• lead to faster utilization of glucose in tissue;
• improve lipoprotein metabolism (increasing the amount of “good” cholesterol and reducing the amount of triglycerides);
• reduce blood viscosity;
• stabilize myocardial function;
• help overcome stress;
• reduce .

However, there are contraindications to performing even simple exercises.

• Glucose less than 5 mmol/l;
• Glucose more than 14 mmol/l;
• High degree of hypertension or hypertensive crisis;
• Decompensation for other concomitant diseases.

Diet therapy for type 2 diabetes mellitus

1. for obese persons, daily caloric intake should not exceed 1800 kcal;
2. you need to eat food often (4-6 times a day) and in small portions (small portions); a diet must be developed to maintain a relatively even level of glycemia;
3. limit the amount of salt consumed to 3 g total, i.e. taking into account the salt contained in prepared products (for example, cheese, bread);
4. limit easily digestible carbohydrates in the diet (flour products, pure sugar, nectars and juices);
5. reduce alcohol consumption to 30 grams or less per day;
6. increase the amount of fiber-rich food consumed (20-40 g per day);
7. The daily required amount of protein is 0.8-1 g/day ( exception: kidney pathology);
8. nutrition balanced in vitamin and mineral composition.

Drug therapy

Despite the fact that lifestyle changes can reliably affect the course of type 2 diabetes, few patients follow the recommendations for a long time. Therefore, drug treatment for type 2 diabetes has become firmly established in medical practice.

According to the mechanism of action, drugs are divided into the following groups:

1. stimulants of insulin secretion (sulfonylureas, glinides);
2. those that eliminate insulin resistance (biguanides, thiazolidinediones);
3. combined (mixed) action (incretin mimetics).

Groups of drugs used for treatment:

• biguanides;
• sulfonylurea derivatives;
• thiazolidinediones;
• prandial regulators;
• alpha-glycosidase inhibitors;
• incretin mimetics;
• insulin preparations.

Biguanides

The only representative is metformin. On sale this is Siofor or Glucophage.

Mechanism of action

This group of drugs is aimed at reducing the body’s resistance to insulin. This is achieved in the following ways:

• the formation of glucose from fats, proteins, as well as in the process of breakdown of liver glycogen is reduced;
• the “storage” of glucose by the liver in the form of glycogen increases;
• the sensitivity of tissue receptors to insulin increases;
• the absorption of sugar into the blood decreases;
• increases glucose consumption by organs and tissues.

Side effects are quite common in this group, and they are all associated with disorders in the digestive tract. However, they go away within 2 weeks, so you need to be patient. If side effects last too long, you should consult a doctor to adjust your treatment. So, the main adverse reactions from metformin include:

• flatulence;
• nausea;
• diarrhea;
• vomit;
• metallic aftertaste in the mouth.

Sulfonylureas

These include the following drugs: glibenclamide, glurenorm, gliquidone.

Mechanism of action

Binds to pancreatic beta cell receptors, stimulating insulin release.
The drugs are prescribed from the smallest dosages, and within one week the dose is increased to the desired level.

The main side effects are: risk of hypoglycemia, itching, skin rash, gastrointestinal disorders, liver toxicity.

Glinids

This group is represented by the drugs nateglinide and repaglinide.

Mechanism of action

Increases the amount of insulin released into the blood by increasing the flow of calcium ions into the cells of the pancreas, which allows control of post-strandial glycemia, i.e. glucose levels after meals.

Thiazolidinediones (glitazones)

The drugs include rosiglitazone and pioglitazone.

Mechanism of action

Medicines in this group activate receptors in muscle and fat cells, increasing their sensitivity to insulin, thereby promoting the rapid utilization of glucose into muscle, fat tissue and the liver.

It should be noted that despite their proven high effectiveness, there are a number of contraindications for their use:

• chronic heart failure (CHF) grade 3-4 according to NYHA;
• increase in liver transaminases in the blood by more than 3 times;
• pregnancy;
• lactation.

Incretin mimetics

The drug in this group is exenatide.

Mechanism of action

There is an increase in insulin secretion under the influence of an increased supply of glucose into the blood, while the process of secretion of glucagon and free fatty acids is suppressed. In addition, the evacuation of food from the stomach slows down, and a person experiences a feeling of fullness longer, so this group belongs to the mixed type according to the mechanism of action.
The main side effect is nausea, which lasts 1-2 weeks from the start of use.

α-glucosidase inhibitors

The only drug represented is acarbose. It is not the mainstay in the treatment of diabetes, but it is quite effective and devoid of such side effects as hypoglycemia due to the fact that it itself is not absorbed into the blood and does not affect the synthesis of insulin.

Mechanism of action

A drug in this group competes with carbohydrates supplied with food for binding to the enzymes of the digestive system responsible for their breakdown. Thanks to this mechanism, the rate of absorption of carbohydrates is reduced, so there is no risk of sudden spikes in sugar after eating food.

Insulin therapy

Insulin therapy has not lost its relevance in the treatment of type 2 diabetes, despite the wide choice of tableted glucose-lowering drugs.

Insulin therapy can be divided by duration:

• temporary;
• constant;

at the start of treatment:

• from the beginning of diagnosis;
• as a result of disease progression (usually after 5-10 years);