Hormonal preparations for parathyroid diseases. Preparations of hormones of the subcutaneous vine

The subhyal gland functions as a gland for extrinsic and internal secretions. The endocrine function is determined by the islet apparatus. Langerhans islands are composed of 4 types of cells:
A (a) clitini, which vibrate glucagon;
In ((3) cells that vibrate insulin and amilin;
D (5) cells that vibrate somatostatin;
F - cells that vibrate pancreatic polypeptide.
The functions of the pancreatic polypeptide are unclear. Somatostatin, which is produced in peripheral tissues (as the body refers to), functions as a paracrine secretion inhibitor. Glucagon and insulin are hormones that mutually regulate the level of glucose in the blood plasma (insulin reduces and glucagon increases). Insufficiency of the endocrine function of the subglottic gland is manifested by symptoms of insulin deficiency (due to which it is considered to be the main hormone of the subglottic gland).
Insulin is a polypeptide that consists of two lancets - A and B, connected by two disulfide sites. Lance A consists of 21 amino acids, Lance B - 30. Insulin is synthesized in the Golgi apparatus (3-clin in the form of preproinsulin and is converted into proinsulin, which is two lances insulin, and receives their lance C-protein, which is formed from 35 amino acid surpluses After the protein is cleaved and 4 amino acid surpluses are added, insulin molecules are formed, which are packaged into granules and subject to exocytosis. It may have a pulsatile nature over a period of 15-30 minutes, and 5 mg of insulin is seen in the systemic circulation, and In total, 8 mg of insulin is present in the subglottic gland (with preproinsulin and proinsulin). Insulin secretion is regulated by neuronal and humoral factors. paracute nervous system(through the mediation of M3-cholinergic receptors) will strengthen, and the sympathetic nervous system (through the mediation of A2-adrenergic blockers) will suppress the production of insulin (3-clits. Somatostatin, which is produced by D-clits, will suppress, and the actions of Monoacids (phenylalanine), fatty acids, glucagon, Amylin and glucose enhances the visible insulin. In this case, the level of glucose in the blood plasma is the primary factor in the regulation of the visible insulin. Glucose penetrates into the third cell and triggers a series of metabolic reactions, As a result, the concentration of ATP in (3-cells) increases. This substance blocks ATP - The stored potassium channels and the membrane (3-clinicals) enter the depolarization state. As a result of depolarization, the frequency of the voltage rise of the stored calcium channels increases. The concentration of calcium ions in P - cells increase, which leads to increased exocytosis of insulin.
Insulin regulates the metabolism of carbohydrates, fats, proteins, as well as tissue growth. The mechanism of insulin infusion into tissue growth is the same as that of insulin-like growth factor (div. Somatotropic hormone). The injection of insulin into carbohydrate metabolism can generally be characterized as anabolic (the synthesis of protein, fat, and glycogen increases), with the primary significance of the injection of insulin into carbohydrate metabolism.
It is extremely important to understand what is included in the table. 31.1 Changes in the metabolism of glucose in tissues are accompanied by a decrease in the level of glucose in the blood plasma (hypoglycemia). One of the causes of hypoglycemia is increased storage of glucose by tissues. The flow of glucose through the histohematic barriers occurs through facilitated diffusion (energy-free transport along an electrochemical gradient through special transport systems). Facilitated glucose diffusion systems are called GLUT. Indicated in the table. 31.1 adipocytes and fibers of transversely mucous membranes contain GLUT 4, through which glucose enters “insulin-dependent” tissues.
Table 31.1. Inject insulin into speech exchange

The infusion of insulin into the metabolism of insulin occurs through the participation of specific membrane insulin receptors. They consist of two a- and two p-subunits, in which the a-subunit is located on the outer side of the membranes of insulin-deposited tissues and forms the binding centers of insulin molecules, and the p-subunit forms a transmembrane domain from them. rosin kinase activity and tendency to mutual phosphorylation . When the insulin molecule is bound to the a-subunits of the receptor, docytosis occurs, and the insulin-receptor dimer is embedded in the cytoplasm of the cell. While the insulin molecule is bound to the receptor, the receptor remains activated and stimulates phosphorylation processes. After the dimer is released, the receptor rotates into the membrane, and the insulin molecule degrades in lysosomes. Phosphorylation processes triggered by activated insulin receptors lead to the activation of certain enzymes

in carbohydrate metabolism and enhancing GLUT synthesis. The process can be schematically represented as follows (Fig. 31.1):
When there is insufficient production of endogenous insulin, diabetes occurs. Its main symptoms are hyperglycemia, glycosuria, polyuria, polydipsia, ketoacidosis, angiopathies, etc.
Insulin deficiency can be absolute (an autoimmune process that leads to the death of the islet apparatus) or temporary (in summer and rural people). In connection with this, it is common to differentiate between type 1 diabetes (absolute insulin deficiency) and type 2 diabetes (absolute insulin deficiency). For both forms Cultural diabetes diet is shown. The order of recognition pharmacological drugs at different forms Diabetes is different.
Antidiabetic products
Status for type 1 diabetes

1. Insulin preparations (substitution therapy)

1. Synthetic antidiabetic products
2. Insulin preparations Insulin preparations

1. Insulin is available in the UK (primarily after 30 months; maximum after 1.5-2 years, initial duration is 4-6 years).
2. Insulin periodic period (beginning after 4-8 years, peak after 8-18 years, final period 20-30 years).
3. Insulin of mid-term duration (beginning after 1.5-2 years, peak after

1. 12 hours, seasonal age 8-12 years old).

1. Medium-grade insulin in combinations.

1. h, reaches a maximum in 7-15 years, lasts 24 years.

The subhyal gland is the external and internal secretion. The endocrine part is represented by the islands of Langerhans; The β-clits of these islands produce insulin, and the α-clits produce glucagon. Prescribed hormones immediately increase the level of glucose in the blood: insulin lowers it, and glucagon increases it. In addition, glucagon stimulates a rapid heart rate.

23.3.1. Insulin preparations and synthetic hypoglycemic agents

Insulin absorbs glucose absorbed by cells in meat and adipose tissue, facilitating the transport of glucose through cell membranes. Changes the level of glucose. Stimulates the creation of glycogen and its production in the liver. In addition, insulin stimulates the synthesis of proteins and fats and prevents their catabolism.

With insufficient insulin production, the level of glucose in the blood rises; there appears in the section, diuresis increases. This type of illness is called blood diabetes (blood diabetes). In diabetic diabetes, in addition to carbohydrate metabolism, fat and protein metabolism are disrupted. Important forms of cardiovascular diabetes will be fatal if treated; death occurs in the stage of hyperglycemic coma (meaning hyperglycemia, acidosis, insomnia, the smell of acetone in the mouth, the appearance of acetone in the mouth, etc.).

Types I and II of blood diabetes are differentiated. Type I diabetes is associated with the destruction of β-clitis in the islands of Langerhans and a significant decrease in insulin levels. In this case, insulin preparations are the only effective means.

In case of diabetes type II, insufficient insulin may cause the following:

1) weakened β-clitin activity and decreased insulin production;

2) decreased strength or sensitivity of insulin receptors; In this case, insulin levels may be normal or may be elevated.

Use synthetic hypoglycemic agents if necessary, take insulin medications.

Insulin medications. Short-term insulin preparations and recombinant insulin preparations for humans. They also use preparations of insulin extracted from the gullet of pigs (porcine insulin).

Insulin should be administered subcutaneously. The effect develops after 15-30 minutes and lasts for about 6 hours. In severe forms of diabetes, insulin is administered 3 times a day: before meals, lunch and evening. at diabetic coma Insulin can be administered internally. Add insulin to the OD; the basic requirement is close to 40 OD.

When an overdose of insulin occurs, instead of glucose in the blood falling below the permissible level, hypoglycemia develops. They appear to be restless, aggressive, sweaty, and more susceptible to hunger; Hypoglycemic shock may develop (loss of speed, blood vessels, impaired heart function). At the first signs of hypoglycemia, a sick person should eat a piece of white bread, baking or zuccor. In cases of hypoglycemic shock, administer 40% glucose (Glucose ♠) internally.

Porcine insulin preparations may cause allergic reactions: infusion at the injection site, blood spray, etc.

Long-acting insulin preparations- different zinc-insulin suspensions - ensure greater absorption of insulin from the place of administration and, at the same time, more troublesome actions.

Medications are divided into mid-life period (18-24 years), long-term (24-40 years).

The duration of drug prescriptions develops stepwise (lasting 6-12 years), so they are unusual for the rapid reduction of hyperglycemia. Administer these drugs only subcutaneously (internal administration is unacceptable).

Synthetic hypoglycemic agents. There are 4 groups of synthetic hypoglycemic agents:

1) derivative sulfonyl compounds;

2) biguanides;

3) thiazolidinediones;

4) α-glucosidase inhibitors.

Compound sulfonyl compounds(Glibenclamide, glipizide, gliclazide, gliquidone, glimepiride) to mean in the middle; stimulate insulin secretion by β-clits of the islets of Langerhans. Increase the sensitivity of insulin receptors to insulin.

The drugs are used for diabetes type II. In case of diabetes type I, it is ineffective.

Side effects: boredom, metal fever in the mouth, pain in the vulva area, leukopenia, allergic reactions. The drugs are contraindicated for impaired liver, liver, and blood system functions.

Biguanides. Stall mostly metformin; recognize in the middle. Suppresses gluconeogenesis (glucose release) in the liver. Reduces absorption of glucose into the intestines. Changes in appetite

reduces excess body weight. Stagnation in case of diabetes type II.

Side effects of metformin: lactic acidosis (elevated level of lactic acid in the blood plasma) - pain in the heart and muscles, pain in the buttocks, as well as metallic fever in the mouth, decreased appetite.

Thiazolidinediones. An apparently new group of antidiabetic agents is also called insulin sensitizers. To avoid increasing the level of insulin in the blood, interact with internal cellular receptors affecting carbohydrate and lipid metabolism. Vicorist drug poglitazone. Used for the treatment of diabetes either in the form of monotherapy or in combination with similar sulfonyl compounds, biguanides, insulin preparations.

α-glucosidase inhibitors. With drugs of this group, stick acarbose(Glucobay *), which has high sporidity to intestinal α-glucosidase, which breaks down starch and disaccharides and absorbs their moistening.

Acarbose is generally considered to be; It inhibits α-glucosidases and thus transfers the absorption of glucose into the intestines.

Side effects: flatulence, diarrhea.

23.3.2. glucagon

Glucagon is a hormone produced by α-clits in the islands of Langerhans, stimulates gluconeogenesis and glycogenolysis in the liver and, in connection with this, increases the level of glucose in the blood plasma. Moves the strength and frequency of the heart; improves atrioventricular conduction. The drug should be administered subcutaneously, internally or internally for hypoglycemia and heart failure.

Antithyroid drugs may stagnate in case of hyperfunction of the thyroid gland (thyrotoxicosis, Graves' disease). At this time, antithyroid drugs are mostly stagnant thiamazole (mercasolil), Which suppresses thyroperoxidase and thus interferes with the iodination of tyrosine excess thyroglobulin and disrupts the synthesis of T 3 and T 4. Meaning. When this drug is ingested, leukopenia, agranulocytosis, skin rash is possible. Possible enlargement of the thyroid gland.

Iodides are generally considered to be antithyroid agents - kaliya iodide or else sodium iodide in high doses (160-180 mg). In this way, iodides reduce the production of thyroid-stimulating hormone by the pituitary gland; The synthesis and production of T 3 and T 4 are significantly reduced. Similar to the mechanism, the suppression of thyroid-stimulating hormone is also avoided when stagnation diiodotyrosine. The drugs will stagnate in the middle. Click for change thyroid gland. Side effects: headache, lacrimation, conjunctivitis, pain in the area linny vines, Laryngitis, skin rash.

3. Preparation for the hormone of parafollicular cells of the thyroid gland

Parafollicular cells of the thyroid gland secrete calcitonin, which prevents decalcification of thyroid tissue, reducing the activity of osteoclasts. The result is a decrease in calcium ions in the blood. a drug calcitonin stagnate with osteoporosis.

Parathyroid hormone preparation

The polypeptide hormone parathyroid hormone parathyroid hormone flows into the exchange of calcium and phosphorus. There is decalcification of bone tissue. Removes the absorption of calcium ions from the scolial-intestinal tract, increases the reabsorption of calcium and reduces the reabsorption of phosphate in nirkov tubules. U vyazku z sim pri dii parathyroid hormone increases the level of Ca 2+ in blood plasma. Medicinal drug for parathyroid lesions of slaughter thinness parathyroidin stagnate with hypoparathyroidism, spasmophilia.

Preparations of hormones of the subcutaneous vine

The subhyal gland is the external and internal secretion. β-clits of Langerhans islands produce insulin, α-clits produce glucagon. Prescribed hormones immediately increase the level of glucose in the blood: insulin lowers it, and glucagon increases it.

1. Insulin preparations and synthetic hypoglycemic agents

Insulin stimulates cell membrane receptors associated with tyrosine kinases. In connection with this insulin:

absorbs the absorption of glucose by tissue cells (behind the central nervous system), facilitating the transport of glucose through tissue membranes;

reduces gluconeogenesis in the liver;

3) stimulates the creation of glycogen and its storage in the liver;

4) promotes the synthesis of proteins and fats and prevents their catabolism;

5) reduces glycogenolysis in liver and skeletal meats.

With insufficient insulin production, diabetes develops, which disrupts carbohydrate, fat and protein metabolism.

Diabetes type I (insulin-dependent) is associated with the destruction of β-clitis in the islands of Langerhans. The main symptoms of type I diabetes are: hyperglycemia, glycosuria, polyuria, sprague, polydipsia (hyperglycemia), ketonemia, ketonuria, ketacidosis. Important forms of diabetes will be fatal without treatment; death occurs in the stage of hyperglycemic coma (meaning hyperglycemia, acidosis, insomnia, the smell of acetone in the mouth, the appearance of acetone in the mouth, etc.). For type I diabetes, the only effective treatment is insulin preparations administered parenterally.

Type II diabetes (insulin-dependent) is associated with changes in insulin secretion (reduced β-clitin activity) or with the development of tissue resistance to insulin. Insulin resistance may be associated with changes in the strength or sensitivity of insulin receptors. In this condition, insulin levels may be normal or may be increased. Increased rhubarb insulin is associated with obesity (anabolic hormone), so type II diabetes is also called regional diabetes. In case of type II diabetes, oral hypoglycemic agents should be used or, if their effectiveness is insufficient, combined with insulin preparations.

insulin medications

Currently, the shortest insulin preparations are recombinant insulin preparations for humans. They also use preparations of insulin extracted from the gullet of pigs (porcine insulin).

Insulin drugs can be produced in humans using genetic engineering methods.

Human insulin(Actrapid NM) is produced in bottles of 5 and 10 ml with 40 or 80 OD per 1 ml, as well as in cartridges of 1.5 and 3 ml for syringe pens. The drug should be administered under the skin 15-20 minutes before taking it 1-3 times a day. The dose should be selected individually depending on the severity of hyperglycemia or glycosuria. The effect develops after 30 minutes and lasts for 6-8 hours. Lipodystrophy may develop in places of advanced insulin injections, so it is recommended to gradually change the place of injections. In diabetic coma, insulin can be administered internally. When insulin is overdosed, hypoglycemia develops. They appear pale, sweaty, very sensitive to hunger, dizziness, heartbeat, restlessness, tremor. Hypoglycemic shock may develop (loss of speed, blood vessels, impaired heart function). At the first signs of hypoglycemia, a sick person should eat sugar, baked goods or other products rich in glucose. In cases of hypoglycemic shock, administer glucagon or 40% of glucose internally.

Zinc suspension of crystalline human insulin(Ultratard NM) inject just under the skin. Insulin is fully absorbed from the subcutaneous tissue; the effect develops after 4 years; maximum effect in 8-12 years; age 24 years old. The drug can be used as a base dose in combination with drugs of rapid and short duration.

Pig insulin preparations are similar to human insulin preparations. However, when they are frozen, allergic reactions are possible.

insulinrozchinnyneutral Available in 10 ml bottles containing 40 or 80 OD per 1 ml. Inject under the skin 15 minutes before meals 1-3 times a day. Possible internal and internal administration.

insulin- zincsuspensionamorphous be administered only under the skin, ensuring greater absorption of insulin from the injection site and therefore a greater effect. The ear will die after 1.5 years; peak after 5-10 hours; Age of age - 12-16 years.

Insulin-zinc suspension, crystalline injected just under the skin. The ear will die in 3-4 years; peak in 10-30 years; age 28-36 years old.

Synthetic hypoglycemic agents

The following groups of synthetic hypoglycemic agents are seen:

1) derivative sulfonyl compounds;

2) biguanides;

Related sulfonyl compounds - butamide, chlorpropamide, glibenclamide recognize in the middle. These drugs stimulate the secretion of insulin by β-clits in the islets of Langerhans.

The mechanism of action of similar sulfonyl compounds involves the blockade of ATP-stored K + channels of β-clin and depolarization of the clit membrane. When this occurs, potential-storage Ca 2+ channels are activated; The input of Ca g + stimulates the secretion of insulin. In addition, this increases the sensitivity of insulin receptors to the action of insulin. It has also been shown that similar sulfonyl compounds promote a stimulating influx of insulin on the transport of glucose in the body (fat, meat). These sulfonyl compounds stagnate in type II diabetes. In case of diabetes type I, it is ineffective. Soak up in the scolio-intestinal tract shvidko and again. A large part is bound to blood plasma proteins. Metabolized in the liver. Metabolites are seen mainly in nircium, but can often be seen in zhovch.

Side effects: boredom, metal fever in the mouth, pain in the vulva area, leukopenia, allergic reactions. Hypoglycemia may occur with overdose of sulfonyl chlorides. The drugs are contraindicated for impaired liver, liver, and blood system functions.

biguanides - metformin recognize in the middle. metformin:

1) increased accumulation of glucose in peripheral tissues, especially meats,

2) reduces gluconeogenesis in the liver,

3) reduces the absorption of glucose into the intestines.

In addition, metformin reduces appetite, stimulates lipolysis and inhibits lipogenesis, resulting in a decrease in body weight. Prescribed for diabetes type II. The drug absorbs well and is effective for up to 14 years. Side effects: lactic acidosis (elevated level of lactic acid in the blood plasma), pain in the heart and muscles, shortness of breath, as well as metallic smell in the mouth, nausea, vomiting, diarrhea.

Preparations of hormones of the subcutaneous vine

The human pod, especially in the caudal part, contains approximately 2 million Langerhans islands, which constitute 1% of its mass. The islets are composed of a-, b- and l-clitins, which secrete glucagon, insulin and somatostatin (inhibiting the secretion of growth hormone).

In this lecture we will highlight the secret of b-clitis of Langerhans' islands - INSULIN, as insulin preparations are currently used as anti-diabetic agents.

Insulin was first seen in 1921 by Banting, Best - for which they were awarded the Nobel Prize in 1923. Isolation of insulin in crystalline form in 1930 (Abel).

Normally, insulin is the main regulator of the level of glucose in the blood. tell slight advancement Instead of glucose in the blood, it stimulates the secretion of insulin and stimulates its further synthesis by b-clits.

The mechanism of insulin binding is that homin enhances the absorption of glucose by tissues and reduces its conversion into glycogen. Insulin, which promotes the penetration of cell membranes for glucose and lowers the tissue threshold to it, facilitates the penetration of glucose into cells. In addition to stimulating the transport of glucose into the cell, insulin stimulates the transport of amino acids and potassium into the cell.

Clints penetrate very well into glucose; In them, insulin has a higher concentration of glucokinase and glycogen synthetase, which leads to the accumulation and storage of glucose in the liver in the form of glycogen. Cream of hepatocytes, glycogen depot and also cells of transverse musculature.

If there is a lack of insulin, glucose will not be readily absorbed by tissues, which will result in hyperglycemia, and with very high levels of glucose in the blood (more than 180 mg / l) and glucosuria (abnormality in the second). i). The Latin name for diabetes is “Diabetes mellitus” (cure diabetes).

The tissue requirement for glucose varies. In a number of textiles

The cerebral cerebellum, the cells of the zoral epithelium, the seminiferous epithelium - the creation of energy is generated only for the growth of glucose. In other tissues, fatty acids can be used to generate energy, in addition to glucose.

In case of celiac diabetes (CD), the situation arises when in the middle of “abundance” (hyperglycemia) the client experiences “hunger”.

In the patient’s body, in addition to carbohydrate metabolism, other types of metabolism are twisted. When insulin is deficient, a negative nitrogen balance is avoided, since amino acids are highly concentrated in gluconeogenesis, which means that amino acids are converted into glucose, and 56 g of glucose are converted from 100 g of protein.

Fat metabolism is also affected, and first of all, it is associated with an increase in the level of free fatty acids (FFA) in the blood, from which ketone bodies (acetoacetic acid) are created. The accumulation of the remainder leads to ketoacidosis all the way to coma (coma - extreme step impairment of metabolism in diabetes). In addition, insulin resistance develops in these brains.

According to WHO data, at this time the number of sick people on the planet reached 1 billion people. Diabetes comes in third place after mortality cardiac-vascular pathologyі evil new creation Therefore, diabetes is one of the most pressing medical and social problems, which will require extreme approaches to resolve.

According to the current WHO classification, the population of patients in the CD is divided into two main types

1. Insulin-dependent cerebrovascular diabetes (previously called juvenile diabetes) - IDDM (DM-I) develops as a result of the progressive death of b-clits, and therefore due to a lack of insulin secretion. This type debuts in children up to 30 years of age and is associated with a multifactorial type of decline, as it is associated with the presence of a number of histosuiciency genes of the first and other classes, for example, HLA-DR4 and HLA-DR3. Individuals with the presence of both antigens -DR4 and -DR3 are at the greatest risk for the development of IDDM. Some patients with IDDM reach 15-20% of the target number.

2. Non-insulin-dependent diabetes mellitus - NIDDM (DM-II). This form of diabetes is called adult-onset diabetes, as it begins after age 40.

The development of this type of diabetes is not associated with the human brain system of histosuction. In patients with this type of diabetes, a normal or moderately reduced number of insulin-producing cells was found in the subslit area, and it is now considered that INCD develops as a result of increased resistance to insulin both functional impairment The ability of b-clin patients to secrete compensatory insulin. Some patients become 80-85% in this form of diabetes.

There are two main types of cream:

3. DM, due to lack of food.

4. Secondary, symptomatic diabetes (endocrine genesis: goiter, acromegaly, disease of the subspot).

5. Vaginal diabetes.

At this time, a new methodology has emerged, a system of principles and views on the care of the sick at the Central Center, the key ones being:

1) compensation for insulin deficiency;

2) correction of hormonal and metabolic disorders;

3) correction and prevention of early and late complications.

Therefore, according to the remaining principles of treatment, the main methods of treating patients with CD will lose the presence of three traditional components:

2) insulin preparations for patients with IDDM;

3) oral sedatives for patients with NIDDM.

In addition, it is important to continue the regime and stage physical requirements. Among the pharmacological agents that are used for the treatment of patients on CD, there are two main groups of drugs:

I. Insulin preparations.

II. Synthetic oral (tablet) antidiabetic agents.

Two hormones vibrate in the subcutaneous vine: glucagon(A-clintins) i insulin(B-clits). The main role of glucagon is to increase the concentration of glucose in the blood. One of the main functions of insulin, however, is to reduce the concentration of glucose in the blood.

Preparations of subglottic hormones are traditionally considered in the context of the treatment of a very important and widespread disease - cardiovascular diabetes. The problem of the etiology and pathogenesis of cellular diabetes is very complex and rich-sided, so here we will pay close attention to one of the key aspects of the pathogenesis of this pathology: impaired ability of glucose to penetrate into the cells. As a result, there is an excess of glucose in the blood, and the cells therefore experience extreme glucose deficiency. The energy supply of cells suffers, the metabolism of carbohydrates is disrupted. Medication-free treatment Cultural diabetes is directly related to this situation.

Physiological role of insulin

The triggering factor for insulin secretion is an increase in the concentration of glucose in the blood. In this case, glucose penetrates through the β-clitin of the subslanous plant and is decomposed by the presence of adenosine triphosphoric acid (ATP) molecules. This leads to the suppression of ATP-stored potassium channels with further disruption of the exit of potassium ions from the cells. The cause is depolarization of the cell membrane, in the process of which potential-stored calcium channels are opened. They enter the body with calcium and, being a physiological stimulator of exocytosis, activate the secretion of insulin into the blood.

Having entered the bloodstream, insulin binds to specific membrane receptors that stabilize the transport complex, which apparently penetrates the entire cell. There, behind an additional cascade of biochemical reactions, membrane transporters GLUT-4 are activated, which are intended for transferring glucose molecules from the blood to the cell. Once glucose has entered the cell, it can be recycled. In addition, in hepatocytes, insulin activates the enzyme glycogen synthetase and inhibits phosphorylase.

As a result, glucose is wasted on glycogen synthesis, and its concentration in the blood decreases. At the same time, hexakinase is activated, which activates the release of glucose-6-phosphate from glucose. The remainder is metabolized in reactions to the Krebs cycle. The outcome of the described processes is a decrease in the concentration of glucose in the blood. In addition, insulin blocks the enzymes of gluconeogenesis (the process of metabolizing glucose from non-carbohydrate products), which also reduces plasma glucose levels.

Classification of antidiabetic conditions

dzherela:
1. Lectures on pharmacology for general medical and pharmaceutical education / V.M. Bryukhanov, Ya.F. Zverev, V.V. Lampatov, A.Yu. Zharikov, O.S. Talalaeva - Barnaul: Spectrum view, 2014.
2. Pharmacology with recipes / Gaev M.D., Petrov V.I., Gayova L.M., Davidov V.S., - M.: ICC Berezen, 2007.