Description:

Carbohydrates are an indispensable and most significant component of food. A person consumes 400-600 g of various carbohydrates per day.
As a necessary participant in metabolism, carbohydrates are included in almost all types of metabolism: nucleic acids (in the form of ribose and deoxyribose), proteins (for example, glycoproteins), lipids (for example, glycolipids), nucleosides (for example, adenosine), nucleotides (for example , ATP, ADP, AMP), ions (for example, providing energy for their transmembrane transport and intracellular distribution).
Numerous disorders of carbohydrate metabolism are conventionally combined into several groups: glycogenosis, hexose and pentosemia, aglycogenosis. The listed disorders are considered as typical forms of carbohydrate metabolism disorders.

Symptoms:

The clinical picture of impaired carbohydrate metabolism is due to the underlying disease.
Examples of some disorders of carbohydrate metabolism:
Glycogenosis is a violation of glycogen metabolism, accompanied by pathological accumulation of glycogen in organs.
Gierke's disease is glycogenosis caused by a congenital deficiency of glucose-6-phosphatase, an enzyme found in liver and kidney cells. Glucose-6-phosphate-za cleaves free glucose from glucose-6-phosphate, which makes possible the transmembrane transfer of glucose from the cells of these organs into the blood. When glucose-6-phosphatase is insufficient, glucose is retained inside the cells. Hypoglycemia develops. Glycogen accumulates in the kidneys and liver, which leads to an increase in these organs. There is a redistribution of glycogen inside the cell towards its significant accumulation in the nucleus. The content of lactic acid in the blood increases, into which glucose-6-phosphate is intensively transferred. Acidosis develops. The body suffers from carbohydrate.
Sick children usually die early. IN 1. The oxidation of pyruvic acid is impaired, since vitamin B1 is part of the coenzyme involved in this process. Pyruvic acid accumulates in excess and partly passes into lactic acid, the content of which also increases. When the oxidation of pyruvic acid is disturbed, the synthesis of acetylcholine decreases and the transmission of nerve impulses is disturbed. The formation of acetyl coenzyme A from pyruvic acid decreases. Pyruvic acid is a pharmacological poison for nerve endings. With an increase in its concentration by 2-3 times, disturbances in sensitivity, neuritis, paralysis, etc.
With hypovitaminosis B1, the pentose phosphate pathway of carbohydrate metabolism is also disrupted, in particular the formation of ribose.
Hyperglycemia - an increase in blood sugar levels above normal. Depending on the etiological factors, the following types of hyperglycemia are distinguished: alimentary, emotional, harmonic, hyperglycemia with anesthesia, with insulin deficiency, etc.

Causes of occurrence:

1. Disorders of hydrolysis and absorption of carbohydrates
2. Violations of the synthesis and breakdown of glycogen
3. Disorders of intermediate carbohydrate metabolism
4. Hyperglycemia

Treatment:

For treatment are prescribed:

The main pathology is treated - diet, drug correction.

Everything in the body should work smoothly and clearly. However, it happens that some organs fail. In this article, I would like to talk about what are the causes and signs of metabolic disorders.

What is metabolism

At the very beginning, you need to understand the concepts that will be used in the article. So what is metabolism? First of all, it is necessary to clarify that another name for this process is metabolism. In essence, this is a certain set of various kinds of chemical reactions, the main purpose of which is to maintain the vital activity of the organism. Other goals and objectives of metabolism:

1. These processes are focused on converting food intake into the body into valuable calories.
2. The next goal flows smoothly from the previous one. The metabolism also "monitors" the expenditure of converted calories.
3. Metabolism synthesizes hormones and enzymes necessary for the body.
4. Also, these processes are responsible for the elimination of decay products.

Metabolism is a process that must be considered not only by the example of the activity of individual organs or systems, but also at the cellular level.

main reason

If a person has a metabolic disorder, the reasons for this can be very different. So, first of all, doctors will trace the patient's heredity. After all, this is what most often leads to the presence of these problems in the patient. However, it should be said that the causes of metabolism have not yet been fully understood and research in this area of \u200b\u200bmedical science is still being actively pursued.

Other reasons

If we talk about such a problem as metabolic disorders, the reasons for this may also be the following:

1. Dysfunction of various organs (pituitary gland, gonads, adrenal glands, thyroid gland).
2. Wrong lifestyle (lack of exercise, alcohol consumption, improper diet - fasting or excessive food intake).
3. Metabolic disorders can provoke certain diseases, as well as stressful situations, physical inactivity, and sleep disturbances.

About violations

What are the signs of metabolic disorders? It is worth saying that with such problems you need to consult an endocrinologist. For example, you can go to the Institute of Endocrinology, where you can get expert advice and assistance. Only specialists will be able to determine what kind of disorder occurs in the patient. These can be carbohydrate, protein, fat, mineral and other disorders. What will be discussed if it is about metabolic disorders? The harmonious interaction of the most important substances that are involved in metabolism is disrupted. What problems can arise in this case?

1. Excess or lack of substances.
2. Various disorders of the digestive reaction.
3. Accumulation of intermediate metabolic products.
4. Unequal formation of metabolic end products.

Violation of protein metabolism

Everyone knows that protein is the most important building material of the human body. Problems with impaired protein metabolism can various diseases and pathology. What, then, will the person feel? The situation automatically falls into two broad categories.

Excess protein

What is the most important symptom of metabolic disorders if you have problems with excess protein? A person will definitely feel a decrease in appetite. Other symptoms:

1. Various intestinal dysfunctions. It can be both diarrhea and constipation.
2. Kidney pathologies may develop, including renal failure.
3. With an excess of protein, the human nervous system is in constant tension. Nervous breakdowns are possible.
4. Salts can be deposited in the patient's tissues.
5. A significant increase in plasma protein is also possible.

Diseases caused by excess protein: arthritis, osteoporosis, gout and obesity.

Protein deficiency

What will a person feel if he has not an excess, but a deficiency of such an important trace element as protein?

1. Weakness, drowsiness.
2. Muscle weakness, hypotonia.
3. Brittle nails, hair, deterioration of the skin.
4. Weight loss (possible weight loss to a state of dystrophy).
5. Also, with a protein deficiency, it will be reduced
6. Frequent infectious diseases, as well as immunodeficiency.

Protein metabolic disorders in children also have certain symptoms. With a protein deficiency, children may have:

1. Lagging in physical development.
2. Mental retardation (decreased intellectual abilities).

Diseases that occur with protein deficiency: kwashiorkor (main symptoms: edema, weakness, weight loss) and alimentary dystrophy (also lack of weight and edema, but also various kinds of immunodeficiency states).

Disorders of carbohydrate metabolism

What are carbohydrates responsible for in the body? Their main task is to nourish the brain cells and carry out the energy function. It is these elements that compensate for the loss of strength and energy during stressful situations or emotional stress. It is also worth saying that problems with carbohydrate disorders of substances accompany the patient most often for life.

Excess carbohydrates

The main symptom of metabolic disorders with problems with carbohydrates is fluctuations in body weight. With an excess of carbohydrates, it can significantly increase, with a deficit, it can decrease. Other indicators:

1. Shivering in the body that comes on involuntarily.
2. Hyperactivity.
3. Hypertension (most often occurs against the background of a significant increase in body weight).
4. An increase in blood glucose levels.
5. Cardiovascular pathologies (most often also occur against the background of obesity).

Diseases that can occur due to excess carbohydrates: obesity and diabetes mellitus.

Deficiency of carbohydrates

The main symptoms that can occur due to carbohydrate deficiency:

1. Depression.
2. Drowsiness, weakness.
3. Weight loss.
4. Tremor of the legs and arms.
5. Decrease in blood glucose levels.

Diseases: hypoglycemia and Gierke's disease.

Fat metabolism disorders

Fats are an equally important element of the human body. It is thanks to fats that the body maintains internal homeostasis. Adipose tissue is found in hormones and nerve fibers.

An important symptom of metabolic disorders in case of a problem with fats is, again, changes in body weight. If we talk about an excess of fat in the body, a person is often diagnosed with obesity. Other symptoms:

1. Atherosclerosis.
2. The formation of stones in the gallbladder and liver.
3. Blood problems: increased clotting, excess cholesterol in the blood.

If we talk about a deficiency of fat in the body, you can observe the following symptoms:

1. Hypovitaminosis.
2. Hair loss.
3. Skin inflammations.
4. Hormonal imbalance.
5. Kidney pathology.

Violation of water exchange

What other symptom of metabolic disorders is there? So, if it is precisely the water exchange that is disturbed, a person may have edema, dropsy, often a state of shock (if we are talking about an excess of water in the body). Loss of electrolytes, disorders of the central nervous system, kidney disease - if we talk about a lack of water in the body.

Violation of mineral metabolism

Minerals are biocatalysts for multiple physiological reactions, as well as stabilizers of the acid state of the body. Most often, various kinds of stressful situations, an unfavorable environment, a too fast pace of life (especially for residents of a metropolis), bad habits, nervousness and, of course, not proper nutrition... When considering endocrine disorders, symptoms of mineral metabolism problems can be as follows:

1. External indicators: brittle nails, acne, hair loss.
2. Insomnia.
3. Decreased immunity.
4. Deterioration of vision.
5. Stool disorders.
6. Decreased libido.

Children

Separately, it is also necessary to consider metabolic disorders in children. It is worth saying that babies can experience similar problems even at a very early age. In this case, it is customary to talk about a disease that is called "exudative diathesis". Main symptoms:

1. Red spots that appear on the baby's body. They can itch, get wet. Similar to Pustules may also appear.
2. Inflammation of the child's eyes, runny nose (problems with mucous membranes occur).

To cope with metabolic problems in children of any age, it is enough just to establish proper nutrition. If we are talking about babies, a nursing mother should correct her diet.

About the types of metabolism

Each person should know what kind of metabolism he has. So, there are three of them:

1. Normal.
2. Accelerated (or fast metabolism).
3. Economical metabolism.

With a normal metabolism, people must follow the diet, since an excess of food can lead to various kinds of problems. If a person has a fast metabolism, then he can eat everything and a lot. And all this is permissible because in their body fats burn faster than accumulate. Those who have an economical metabolic regime, as they say, "get fat from water." Such people should carefully monitor their diet, not allowing themselves anything unnecessary. However, how can you know what kind of metabolism a person has? There are two ways.

1. Conduct a biochemical study of the body. Disadvantage: the high cost of the procedure.
2. Conduct a little experiment.

About the experiment

In order to find out what kind of metabolism a person has, it is not necessary to visit the Institute of Endocrinology. In this case, you can use a proven method. To do this, you need to get up in the morning (preferably on Sunday), do all the hygiene procedures. After going to the kitchen, you need to warm up and quickly eat 300 g of porridge. Then you need to wait a couple of minutes.

1. With an accelerated metabolism, sweat will appear.
2. If it gets warm, the metabolism is normal.
3. If a person does not feel or sense anything at all, he has an economical type of metabolism.

Prevention

Preventing metabolic disorders is a great way to avoid metabolic problems. What will be relevant in this case:

1. Proper balanced nutrition. It is necessary to give up starchy, fatty, sweet foods to the maximum. You can't overeat or starve. You also need to ensure that the body consumes all vitamins and minerals in full.
2. The body must rest properly (uninterrupted 7-hour sleep is important).
3. You need to try to avoid stressful situations and emotional overload.
4. You need to completely get rid of all bad habits.
5. It is also advisable to avoid adverse environmental factors.

In this case, the prevention of endocrine diseases will also be important. Particular attention should be paid to preventive measures for diabetes and hypoglycemia (carbohydrate imbalance).

Treatment

So, we found out what a metabolic disorder (symptoms) is. Treatment of this problem is what I also want to talk about. You can cope with metabolic disorders with the help of various kinds of medications.

1. Stimulants containing caffeine and theine (most commonly used by athletes).
2. Hormonal drugs, as well as medicines that treat endocrine disorders.
3. Drugs based on antidepressants.
4. Various kinds of extracts. For example, guarana extract, which normalizes cell metabolism and accelerates

ethnoscience

Important: if a person has certain metabolic problems, then it is best to seek help from a qualified specialist. Otherwise, you can do great harm to your health. However, if there is no way to go to doctors, you can try to cope with the problems with traditional medicine:

1. To restore metabolism, you can prepare an infusion of walnut leaves. To prepare the medicine, you need to take two teaspoons of dry leaves, pour one glass of boiling water and leave everything for about an hour. The broth should be taken 4 times a day, half a glass before meals.
2. You can drink horsetail tea (available at the pharmacy). For medicinal purposes - three times a day for a quarter of a glass. It will help not only adjust the metabolism, but also cleanse the body.
3. And to just go to the sauna or bath regularly. However, you first need to make sure that there are no other contraindications to their visit.

Metabolism is one of the main functions of the body, during which transformation occurs chemical substancesthat ensure the growth, development and vital activity of cells. In case of metabolic disorders during internal organs their functioning changes and the relationship of the body with the environment becomes more complicated, as a result, the production of hormones and other necessary substances worsens, which provokes the appearance of symptoms of severe diseases of the endocrine and reproductive systems.

What is metabolism

Metabolism is a complex of chemical reactions that take place in the cells and intercellular fluid of the body. Thanks to the constantly acting metabolism, human life is supported. Metabolism allows the body to develop, multiply, maintain all its functions and adequately respond to the effects of the external environment. This complex chemical process involves proteins, fats, carbohydrates and many other elements, each of which plays a specific role in metabolism. Metabolism is carried out in the following stages:

• nutritional components enter the human body;
• they are absorbed from the digestive system, fermented, broken down into smaller components and penetrated into the circulatory system;
• substances are transported, assimilated by different organs and systems, release energy;
• decay products that the body has not absorbed are removed through the lungs, intestines, and excretory system.

This pathology represents changes in one of the metabolic stages - in anabolism or catabolism. The latter is the oxidation or differentiation of complex elements to the state of simple organic molecules capable of participating in anabolism - synthesis, which is characterized by energy consumption. An abnormal metabolism is characterized by a too slow or accelerated metabolic rate.

A low metabolic rate implies that metabolic processes are slow: fewer calories are burned in a given time than needed, while the transformation of nutrients into energy is also slowed down. So, a person develops problems with being overweight, since not all calories consumed have time to burn, instead being deposited in the form of fatty folds on the body.

An accelerated metabolism is also a disorder in which a person consumes almost any food, but is not able to gain the optimal weight for himself. Useful elements and vitamins that enter the body with food are not absorbed. As a result, a deficiency of important enzymes is formed, which slows down the work of key body processes. A person with a fast metabolism often does not feel well, because his immunity is weakened. This reduces the body's resistance to seasonal illness.

Causes

A common factor in metabolic disorders is hereditary metabolic disorders. The key role in the regulation of intracellular metabolism is played by genetic information: when genes are mutated (especially those responsible for coding for enzyme synthesis), metabolic defects develop. In addition, gene (congenital) defects cause mutations in structural and transport proteins. Metabolic diseases can be associated with:

• pathological changes in the functioning of the thyroid gland;
• malfunctioning of the adrenal glands or pituitary gland;
• improper diet (overeating, starvation, diet);
• non-compliance with a healthy lifestyle (the presence of bad habits, physical inactivity, etc.);
• improper sleep patterns.

Symptoms

Signs of abnormal metabolism can be different, they depend on the level at which changes occur - molecular, cellular, in tissues, organs or throughout the body as a whole. Any failure of the chemical metabolic process can cause endocrine diseases, dysfunction of various organs / systems, hormonal failure. Changes in the body appear gradually, so the primary symptoms are often invisible.

Metabolic disorders show a variety of symptoms, among which obesity is common. Other signs of the presence of pathology are:

• changes in the structure of the skin;
• fragility of hair, nails;
• swelling;
• severe weight gain or loss;
• increased appetite or lack of it;
• the appearance of dermatological problems - skin rash, acne, etc.;
• the appearance of hypo- or hypergmentation;
• problems with teeth (destruction of enamel);
• pallor of the skin, swelling of the limbs, puffiness of the face;
• digestive disorder (diarrhea alternates with constipation).

Violation of carbohydrate metabolism

The main task of carbohydrates in the body is to nourish brain cells and replenish energy. Carbohydrate compounds compensate for the loss of strength during emotional or stressful stress. At the same time, problems with the absorption of carbohydrates, as a rule, accompany the patient for life. The main symptom of a carbohydrate metabolism disorder is weight fluctuations. When the norm of carbohydrates is exceeded, the mass increases, with a shortage it decreases. Other symptoms of a carbohydrate disorder:

• involuntary tremors in the body;
• hyperactivity;
• cardiovascular diseases;
• hypertension (with obesity);
• diabetes;
• increased blood glucose levels;
• depression;
• weakness / drowsiness;
• loss of body weight;
• gierke's disease;
• hypoglycemia.

Protein metabolism

Protein is the main building material in the human body. Various pathologies can serve as the cause of problems with impaired protein metabolism. With an excess of protein in humans, there is:

• decreased appetite;
• stool disorder (constipation, diarrhea);
• kidney pathology, organ failure;
• stressful state of the nervous system (nervous breakdowns may occur);
• deposition of salts in tissues;
• an increase in the amount of protein in the blood plasma.

Deterioration in the digestibility of protein foods, in which the body accumulates a large number of amino acids and other constituent elements, causes a number of diseases, including fatty liver disease, osteoporosis, obesity, gout. With too rapid breakdown of proteins and their deficiency in the body, a person experiences:

• hypotonia, weakness;
• deterioration of the condition of the skin, hair, nails;
• rapid weight loss;
• wasting muscle tissue;
• decreased performance;
• immunodeficiency.

Fat metabolism

The balance of fats ensures that the body is able to maintain normal homeostasis. Adipose tissue is found in hormones and nerve fibers. The main symptom of a violation of fat metabolism is a change in body weight. With an excess amount of a substance, a person has:

• blood problems (excess cholesterol, increased clotting);
• atherosclerosis;
• the formation of stones in the liver, gallbladder;
• obesity.

With a deficiency of fat, liver functions suffer, and diseases of the kidneys and other organs can develop. Symptoms of low fatty acids include:

• skin inflammation;
• hypovitaminosis;
• hormonal imbalance;
• hair loss;
• underweight.

Water exchange

Water is the most important component of homeostasis; more than half of the human body weight consists of it. Normal fluid balance means almost equal intake and removal of fluid from the body. Violation of this indicator can occur with the following symptoms:

• thickening of the blood;
• the development of diseases of the gastrointestinal tract and central nervous system;
• swelling of the skin;
• dysfunction of the excretory system;
• increased pressure;
• decrease in cardiac output, etc.

Mineral exchange

Minerals act as biocatalysts for many physiological processes and the acid state of the body. As a rule, stressful situations, an accelerated pace of life, an unfavorable environment, bad habits and an unbalanced diet lead to a violation of the mineral balance. If metabolism is impaired due to endocrine abnormalities, the following symptoms may occur:

• decreased immunity;
• insomnia;
• deterioration of vision;
• brittle nails;
• decreased libido;
• upset stool;
• hair loss;
• acne eruptions.

In children

This problem can occur in a child at a very early age. To restore normal metabolism, you should establish proper nutrition for the baby. In violation of metabolic processes in children, the doctor diagnoses "exudative diathesis", the main signs of which are:

• red spots on the body that can get wet and itchy;
• pustules on the skin;
• runny nose, eye inflammation.

Diseases associated with metabolic disorders

Metabolic failure is associated with a violation of the normal processing of fats by the liver. At the same time, there are fewer low-density lipoproteins in the blood and the body begins to form reserves. A person's blood vessels suffer, which over time will lead to stroke and heart disease. Metabolic disorders are often associated with other medical conditions, including:

1. Gierke's disease. Congenital metabolic disorders, in which glycogen accumulates in the tissues excessively. Pathology manifests itself in infants with growth retardation, an increase in the size of the liver, and a protrusion of the abdomen. The only treatment for Gierke's disease is diet. With age, the patient's condition improves.
2. Phenylketonuria. This is a hereditary pathology characterized by a slowdown in mental development. It arises due to a deficiency of the enzyme responsible for the conversion of phenylalanine to tyrosine.
3. Alcaptonuria. The disease is caused by a genetically determined deficiency of an enzyme that is involved in the metabolism of homogenous acid. As a result, arthritis develops. For therapy, a diet is prescribed, implying the rejection of products with tyrosine and phenylalanine.
4. Albinism. This is a congenital absence of the skin black pigment melanin (typical for albinos).
5. Gout. Chronic disease caused by impaired metabolism of salt, endogenous uric acid. Gout is characterized by the deposition of the mineral in the kidneys, joints and cartilage, which causes painful inflammatory edema to form.
6. Hypercholesterolemia. The inability of the body to break down lipoproteins and zolesterol, which leads to the accumulation of these substances in the tissues. The disease causes atherosclerosis.

Treatment

Therapy should begin with eliminating the causes that caused it. To do this, adjust the diet and diet, reducing the amount of consumed carbohydrates and fats. Patients regulate the mode of wakefulness and rest, strive to avoid stress, go in for sports, which increases energy metabolism and the body becomes in good shape. The listed measures help to eliminate metabolic disorders that are not complicated by genetic or other factors.

If the problem is neglected, you cannot do without medical help. If the pathology has already affected the work of organs, the patient needs to undergo a course of treatment, including the reception:

• hormonal drugs (with an imbalance of hormones);
• thyroid medications (in case of malfunction of the thyroid gland);
• insulin (for diabetes).

Drugs

Decreased or increased metabolism suggests complex treatment carried out under the supervision of a physician. Drugs that help correct metabolism are divided into the following categories:

1. Hormones. Means based on biostimulants that normalize metabolism. Appointed only after diagnostics.
2. Vitamin complexes. Preparations containing active compounds that take part in all vital processes, including fermentation, energy storage, production of necessary substances, tissue development, etc. Vitamins are taken regularly according to the doctor's prescribed dosage and scheme.
3. Enzymes. Products that neutralize the viscous consistency of hyaluronic acid.
4. Medicines that control hemostasis. Antrombiotics, stimulants of erythropoiesis, hemostatics, etc.
5. Amino acids (glycine, methionine). Means that compensate for the deficiency of these substances in the body, improving the state of energy resources, adjusting hypothalamic-pituitary activity, etc.
6. Biostimulants. They improve the state of the nervous system, activate the protective properties of the body, and eliminate hypoxia. These drugs slow down or speed up metabolism, bringing it back to normal, have a reparative effect.

After examining the patient and determining the causes of the pathology, doctors prescribe certain medications. As a rule, several of the most effective drugs are prescribed, for example:

1. Reduksin. This drug is suitable for patients in whom metabolic failures have led to gluttony and constant hunger. The components included in Reduxin give a feeling of satiety and help slow down the absorption of food, improving digestion. As a result, a person consumes a normal amount of food for him and gradually gets rid of the extra pounds gained during the illness.
2. L-thyroxine. The medicine has a similar effect with the thyroid hormone and is prescribed for pathologies caused by its dysfunction. After taking the drug, the work of the gland improves, the metabolism returns to normal.
3. Glucophage. The medication normalizes the functioning of the pancreas, preventing the release of excess insulin into the blood, which is often observed with improper metabolism.

Diet

Abnormalities in metabolism require dietary adherence. For adults, the doctor prescribes food No. 8 according to Pevzner. Eating overweight and obesity is suitable for almost all people with impaired metabolism. The principle of the menu is not about reducing calories, but about restoring the function of systems and organs. A key sign of the effectiveness of the diet for metabolic disorders is the state of feeling of mild hunger.

The daily calorie content of the proposed diet is 2000 kcal, while the weight is normalized gradually and without harm to health. Basic diet rules:

• bread can only be made from coarse flour, no more than 150 g per day;
• you should eat vegetables daily (at least 200 g), with the exception of potatoes, beets, carrots;
• the patient's menu includes liquid soups in lean broth, but first courses with pieces of lean meat or meatballs are allowed twice a week;
• it is necessary to refuse spicy, salty, pickled food;
• allowed to eat pasta from durum wheat 2 times a week (portion no more than 150 g);
• lean meat should be in the diet every day, not less than 150 g each (can be replaced with fish);
• eggs are allowed, but not more than 1 per day;
• only vegetable oil is allowed;
• tea and weak coffee are drunk without sugar;
• consumption of fruits is compulsory, with the exception of bananas and grapes;
• low-fat dairy products are allowed;
• baked goods, sweets are prohibited;
• be sure to drink 1.5-2.5 liters of water per day;
• animal fats, rice, legumes, alcohol, store sauces, smoked meats, semolina, sausages are prohibited.

Folk remedies

If you have problems with metabolism, you must definitely contact a specialist, otherwise there is a risk of worsening your own condition. In addition to the prescribed treatment, it is allowed to use folk methods therapy. The following are considered effective:

1. Infusion of walnut leaves. Four teaspoons of dry leaves are poured into 400 ml of boiling water, infused for an hour. The broth is taken in ½ tbsp. 4 times a day before meals.
2. Horsetail tea. 1 tsp herbs are brewed with a glass of boiling water and insisted for 15 minutes. Tea is drunk 3 times a day for ¼ st.
3. Garlic tincture. 350 g of the product is grated, then 200 ml of alcohol is poured into the lower part of the mass (where there is more juice) and placed in a cool dark place for 10 days. After that, the liquid is drained and drunk daily: first 2 drops, but every day increasing the dosage by another 2 drops. The duration of the course is 11 days.

Prevention

To prevent metabolic failure, it is important to constantly supply your own body with the necessary substances. In this case, oxygen takes a special place: with a sufficient amount of it in the body, metabolic processes are activated. Other measures for the prevention of pathology are:

• taking vitamin and mineral complexes;
• regular sports;
• compliance with optimal sleep and rest;
• balanced diet;
• the desire to avoid stressful situations and overwork;
• rejection of bad habits.

Video

The human body is a complex mechanism, within which many different processes take place, aimed at ensuring its normal life. The most important role in this is played by carbohydrate metabolism, and the value of carbohydrates depends on their energy function. In this case, glucose acts as a source of energy for the entire body.

In the event that energy costs begin to increase rapidly in the body, then this ensures the timely readiness of all energy resources. But with a decrease in glucose levels, it is quite possible that the central nervous system will suffer. So, with hypoglycemia, a person will quickly get tired and feel weak throughout the body.

Carbohydrate metabolism in the body is the process of breaking down carbohydrates in order to form certain end and intermediate products. In addition, during the exchange, some substances are converted into others. Thus, simple carbohydrates become more complex during metabolism. But sometimes there is a violation of carbohydrate metabolism, which occurs for a variety of reasons.

Usually, the process of absorption of carbohydrates is disrupted due to the formation in the gastrointestinal tract of amylolytic enzyme deficiency. At the same time, carbohydrates entering with food do not fall under the breakdown to the level of monosaccharides, which means they are not absorbed. If the violation is prolonged, then carbohydrate starvation gradually develops. Also, impaired absorption of carbohydrates occurs when poisoning with poisons that block hexonisane, and this stops the phosphorylation of glucose, which does not enter the bloodstream. But carbohydrate metabolism is important for human life.

Disorders of glycogen synthesis and splitting can often be found, which is directly related to the process of carbohydrate metabolism. In this case, glycogen synthesis is capable of pathologically weakening or increasing. If the central nervous system is agitated, then the decay is enhanced. In the event that its deficiency is observed, the body will consume energy through fat oxidation, which means that carbon and fat metabolism will occur. All this can lead to a deterioration in well-being and weight loss.

But most of all, insulin influences the process of carbohydrate metabolism. That is why a violation of carbohydrate metabolism is a sign of the onset diabetes mellitus... This disease is very common, and many methods are used to treat it. As a preventive measure, it is possible to use medications Spirulina, Fucoxan, Dilitovit and Suga Balance. As practice shows, such prevention is very effective and takes into account all the features of the course of carbohydrate metabolism.

During diabetes mellitus, the regulation of carbohydrate metabolism usually suffers, and this leads to negative consequences. The level of glucose in the blood rises significantly, which is no longer absorbed into the tissue, which means that it accumulates in the bloodstream. At the same time, the body does not receive the required amount of energy, which promises disruptions in its work. Due to changes in the brain when there is no glucose, a person may fall into a coma. Timely recognized symptoms are able to provide effective treatment, but only on condition of timely referral to a specialist.

Carbohydrates have always been a significant and indispensable component of food. Being a necessary participant in metabolism, carbohydrates are included in all types of metabolism: proteins (in the form of glycoproteins), nucleic acids (in the form of deoxyrbose and ribose), nucleosides (adenosine), lipids (glycolipids), nucleotides (ATP, AMP, ADP), ions (provide energy for their intracellular distribution and transmembral transfer).

All disorders of carbohydrate metabolism are conventionally divided into several groups: hyperglycemia, hypoglycemia, aglycogenosis, glucosemia, pentosemia. All these disorders are considered typical forms of carbohydrate metabolism disorders.

Symptoms of carbohydrate metabolism disorders largely depend on the disease. So, glycogenosis is a violation of glycogen metabolism, which is accompanied by pathological accumulation of glycogen in the organs. In Gierke's disease, glycogenosis occurs, which is caused by a congenital deficiency of an enzyme found in the cells of the kidneys and liver - glucose-6-phosphatase. This component cleaves free glucose, which makes it possible to transfer glucose from organs to the blood. If glucose-6-phospatase deficiency occurs, then glucose is retained inside the cells, which develops hypoglycemia. Glycogen accumulates in the kidneys and liver, and this leads to an increase in these organs. Thus, there is a redistribution of glycogen in cells towards its accumulation in the nuclei. This causes the lactic acid content in the blood to rise, which means that it leads to the development of acidosis. The body begins to suffer from carbohydrate starvation and children die quickly.

With hypovitaminosis B1, there is a violation of the oxidation of pyruvic acid, since vitamin B1 is included in the composition of the coenzyme, which is involved in this process. In excess, pyruvic acid accumulates, and it partially passes into lactic acid, whose content also increases. Such a violation of the oxidation of pyruvic acid leads to a decrease in the synthesis of acetylcholine, as well as to a violation of the transmission of nerve impulses. Pyruvic acid is a nerve poison. And with an increase in three times its concentration, disturbances in sensitivity, paralysis, neuritis and so on occur.

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Karaganda State Medical University

Department of Pathological Physiology

abstract

Ontopic: "Violation of carbohydrate metabolism»

Completed: student of group 2-095 OM

E.V. Nedorostkova

Checked by: teacher

Mokhir Yu.M.

Karaganda 2015

Introduction

The advances in medicine in recent decades have led to a sharp decline in infectious diseases. However, the overall morbidity of the population remains high due to the growth of the so-called diseases of civilization. Among the various reasons for the increase in the number of these diseases, various metabolic disorders come out on top.

Many pathological processes and diseases inevitably affect the course of metabolic reactions and can themselves cause and trigger disturbances in acid-base, water-electrolyte and carbohydrate homeostasis in the body. Since there are close interrelationships between various metabolic reactions and pathways, changes in metabolic processes are rarely isolated and often represent a complex of interdependent and interrelated pathophysiological processes. As a typical example, diabetes mellitus can be cited, in which not only the metabolism of carbohydrates is disturbed, but also the metabolism of lipids, proteins, acid-base and water-electrolyte balance is disturbed.

Of all metabolic disorders, carbohydrate suffers first of all, as the most significant in the energy supply of the body and the most labile in relation to various external and. internal factors.

Disorders of carbohydrate metabolism can manifest themselves at various levels of biological organization - from molecular to organismal. They can arise as a result of a violation of neuro-hormonal regulation, genetic information, or the direct action of pathogenic factors.

The basis for disorders of carbohydrate metabolism is primarily living conditions modern man: overstrain of the nervous system, physical inactivity, unbalanced nutrition and others, which can cause the development of many pathological processes and diseases (for example, exudative diathesis, dental caries, obesity, vascular lesions, etc.). The most frequent and severe form of carbohydrate metabolism pathology is diabetes mellitus, which affects about 4% of the population. Diabetes mellitus is in third place in mortality, and in first place in disability, in particular in blindness.

Knowledge of the etiology and mechanisms of carbohydrate metabolism disorders is a prerequisite for a deep understanding of clinical manifestations, diagnosis and pathogenetic therapy of metabolic and endocrine system diseases.

1. Common pathogen without disorders of carbohydrate metabolism

Carbohydrates in the human body are present in a much smaller amount (no more than 2% of dry body weight) than proteins and lipids. In the body, carbohydrates perform a variety of functions, the most important of which are energy (the main source of energy for cells) and structural (an essential component of most intracellular structures). In addition, carbohydrates are used for the synthesis of nucleic acids (ribose, deoxyribose), and also form compounds with protein (glycoproteins, proteoglycans), lipids (glycolipids) and other substances (heteromonosaccharides), being components of many enzymes and regulatory systems that provide numerous specific functions ...

Chemically, carbohydrates are aldehydes and ketones of polyhydric alcohols. Monosaccharides combine through a glycosidic bond to form disaccharides, oligosaccharides (3 to 6 monosaccharide residues) and polysaccharides (glycogen, starch). The most common in the body are pentoses (which are part of nucleic acids and many coenzymes, in particular NADP) and hexose (glucose, fructose, galactose). For energy metabolism, glucose is of the greatest importance. Firstly, it is the only source of energy for the central nervous system, in which there are no energy reserves and it does not use other sources of energy, for example, proteins and fats (with the exception of ketone bodies during starvation). Secondly, the body creates a reserve of glucose in the form of glycogen, which is rapidly broken down and supplies glucose to the blood. Thirdly, for the complete oxidation of 1 glucose molecule (to CO2 and H2O, which are easily removed from the body), less oxygen is required than for the oxidation of fatty acids, and the yield of macroergs is significant: 38 ATP molecules.

In the metabolism of carbohydrates, it is customary to distinguish the following stages:

digestion and absorption of carbohydrates in the gastrointestinal tract;

the processes of synthesis and cleavage of glycogen;

intermediate metabolism of carbohydrates and their utilization in tissues.

Causal factors that disrupt carbohydrate metabolism can manifest themselves at each of these stages of carbohydrate metabolism.

Regulation of carbohydrate metabolism

2. Impaired digestion and absorption of carbohydrates in the digestive tract

Dietary glycogen and starch account for 60% of the incoming carbohydrates. The rest of the consumed carbohydrates are natural disaccharides (sucrose, maltose, lactose) and, to a lesser extent, monosaccharides (glucose, fructose). Various hereditary or acquired causes can interfere with the breakdown of carbohydrates and the absorption of glucose. The consequence of this on the part of the gastrointestinal tract is flatulence and osmotic diarrhea, and on the part of the blood, especially on an empty stomach, hypoglycemia. Under these conditions, gluconeogenesis prevents the body from dropping too much blood glucose. This type of carbohydrate metabolism disorder is discussed in more detail in the course of private pathophysiology.

Violation of the synthesis and splitting of glycogen, glycogenosis.

In cells, glucose coming from the blood is phospholyzed to hexokinethe heat of the reaction, turning into glucose-6-phosphate (Gl-6-F). From Gl-6-F, as a result of the combined action of glycogen synthetase and the "branching" enzyme, glycogen is synthesized - a polymer, the molecule of which can contain up to a million monosaccharides. In this case, a kind of crystallization of glycogen occurs, as a result of which it does not have an osmotic effect. This form is suitable for storing glucose in the cell (if the same number of glucose molecules were simply dissolved in the cytoplasm of the cell, the cell would inevitably be destroyed due to osmotic forces).

Glycogen is found in the cells of all tissues. Most of it is in the liver and muscles, while in the cells of the nervous system it is present in minimal amounts. The rate of glycogen breakdown is determined by the needs of the body. Under normal conditions, the breakdown of glycogen provides a daily entry into the bloodstream of 1.9 to 2.1 mg of glucose per kilogram of body weight. The main supplier of glucose formed from glycogen is the liver, since its cells, unlike muscle cells, are able to hydrolyze glucose-6-phosphate to glucose.

Strengthening the breakdown of glycogen. In the muscles, intense glycogenolysis occurs with severe physical exertion. Part of glucose is metabolized to CO 2 and H 2 O with the formation of the maximum amount of ATP, and part to lactic acid, which enters the bloodstream, to the liver and can be resynthesized there into glucose. In the liver, glycogenolysis is activated in response to a decrease in serum glucose concentration or as a component of a stress response. The main hormones that activate glycogenolysis are glucagon, adrenaline and cortisol. To a lesser extent, activation of glycogenolysis is facilitated by conditions accompanied by hyperproduction of STH and thyroid hormones. The activation of the sympathetic nervous system also promotes glycogenolysis. The consequence of the activation of glycogenolysis is an increase in the level of glucose in the blood.

Weakening of glycogen synthesis is noted during hypoxia, because it disrupts the formation of ATP, which is necessary for the formation of glycogen. Since the main place of synthesis and accumulation of glycogen is the liver, its severe lesions, accompanied by inhibition of glycogen-forming function, lead to a pronounced decrease in total glycogen reserves.

Insufficient glycogen content in its main depot, i.e. in the liver, prevents the elimination of hypoglycemia with insufficient intake of glucose from food (fasting, gastrointestinal tract pathology) or with its active consumption (muscle load, stress). In conditions of a deficiency of exogenously supplied glucose and a decrease in its endogenous reserves deposited in the form of glycogen, energy metabolism begins to be provided by proteins and fats. This is accompanied by the loss of plastic material, as well as the accumulation of ketone bodies, which provoke acidosis and intoxication.

Excessive accumulation of glycogen due to the weakening of its utilization is observed in glycogenosis.

Glycogenosisare a group of rare hereditary diseases in which, due to enzyme defects, either the breakdown of glycogen, which has a normal structure, is inhibited, or glycogen is initially formed with an altered structure, which prevents its subsequent breakdown. In either case, an excess supply of glycogen is deposited in the organs. At the same time, against the background of significant reserves of endogenous glucose deposited in glycogen, due to the impossibility of using it, patients develop severe hypoglycemia. To date, 12 types of glycogenosis have been identified. As an example, consider one of the 6 most common glycogenoses.

The most common forms of glycogenosis

Manifestations of glycogenosis:

Clinical:

deposits of glycogen in various tissues and organs (liver, kidneys, skeletal muscles, myocardium) with impaired functions;

muscle weakness;

developmental delay

Laboratory:

hypoglycemia, increased insulin sensitivity;

a tendency to lactate and ketoacidosis;

with a test with glucagon or adrenaline, not hyperglycemia (a normal reaction due to the activation of glycogenolysis) is noted, but an increase in blood lactate and pyruvate.

Type I glycogenosis (Gierke's disease) occurs when there is a congenital deficiency in the liver and kidneys of the enzyme glucose-6-phosphatase. This enzyme cleaves free glucose from GL-6-F, which makes it possible for its transmembrane transition from liver and kidney cells to the blood. With a deficiency of glucose-6-phosphatase, glycogen, which has a normal structure, accumulates in the cells of the liver and kidneys. Hypoglycemia develops, insulin sensitivity increases. The content of ketone bodies increases, which is a consequence of the activation of fat metabolism and lipid oxidation during hypoglycemia. Thus, metabolic lactate and ketoacidosis develops. Pathological symptoms appear already in the first year of a child's life: the liver and kidneys are enlarged, growth retardation is observed, as a result of hypoglycemia, convulsions may occur. Sick children, as a rule, die early from intercurrent

(additionally developing) diseases and acidotic coma. The disease is inherited in an autosomal recessive manner.

3. Intermediate carbohydrate metabolism disorders

Intermediate metabolism of carbohydrates is understood as the processes of their transformation in tissues, closely related to protein and lipid metabolism and aimed both at creating conditions for maintaining an adequate energy metabolism and at the formation of a number of compounds necessary for the body. The latter include pentose phosphates (used for the synthesis of nucleotides and NADPH), as well as numerous heteropolysaccharides that act as neurotransmitters in the body (acetylcholine), antioxidants (glutathione), biologically active substances (heparin and other proteoglycans), secretory components (mucopolysaccharides), etc. ...

The following processes and conditions can be cited as examples of manifestations of disorders in intermediate carbohydrate metabolism:

Increased glycolysis under hypoxic conditions;

Inhibition of the formation of acetyl-CoA;

Abnormal changes (excessive increase and decrease) in gluconeogenesis activity;

Defects in the pentose phosphate pathway of carbohydrate utilization.

In hypoxic conditions (against the background of general insufficiency of blood circulation, respiration, with severe anemia, etc.) due to the predominance of anaerobic respiration over aerobic respiration, an excessive accumulation of lactic and pyruvic acids occurs, which provokes tissue acidosis. Excessive mobilization of glycogen as a source of glucose under conditions of its ineffective anaerobic utilization leads to depletion of glycogen stores during chronic hypoxia, which further contributes to hypoglycemia.

Blocking the formation of acetyl-CoA leads to a violation of the interconversions of carbohydrates, fats and proteins, since all such interconversions must go through the intermediate stage of acetyl-CoA. The latter is formed in mitochondria as a result of oxidative decarboxylation of pyruvic acid. Hypoxia, arsenic intoxication, some hypovitaminosis (for example, lack of vitamin B 1 - thiamine) damage the pyruvate dehydrogenase system and reduce the synthesis of acetyl-CoA. Because of its universal role, it affects a variety of cells, tissues, and organs, from red blood cells to the central nervous system.

Deviations in the activity of gluconeogenesis always noticeably affect the level of glucose in the body. This process is an additional source of endogenous glucose due to its synthesis from glycogenic amino acids (alanine, glycine, serine, etc.), lactic and pyruvic acids, glycerol and a number of other compounds in liver and kidney cells.

Gluconeogenesis is mainly activated (enhanced) in cases where the utilization of glycogen is insufficient to maintain blood glucose levels that can satisfy the body's needs. Similar cases are observed during periods of prolonged fasting, with prolonged and hard physical work.

The main hormonal stimulants of gluconeogenesis are glucocorticoids and glucagon. Adrenaline, growth hormone and thyroid hormones also contribute to the activation of gluconeogenesis, since they increase lipolysis, i.e. increase the level of fatty substrates that are converted into carbohydrates. An increase in the production of these hormones is accompanied by an increase in gluconeogenesis and, as a consequence, hyperglycemia. The downside of enhanced gluconeogenesis is the catabolism of fats and proteins (in lymphoid tissue, skin, muscles), which supplies substrates for glucose synthesis.

Inhibition of gluconeogenesis with the development of hypoglycemia is noted with a deficiency of the above hormones, with excessive production of insulin (with insulinoma), as well as with severe liver damage.

Violations of the pentose cycle of glucose oxidation can be acquired (with a deficiency of vitamin B 1, when the formation of ribose is disturbed) or congenital. Among congenital defects of the pentose-phosphate shunt, the most common deficiency or abnormality of glucose-6-phosphate dehydrogenase. At the same time, the necessary restoration of glutathione, which is the most important factor in antioxidant protection, is not provided. In the erythrocyte membrane, glutathione deficiency is accompanied by the activation of lipid peroxidation, which entails an increase in membrane permeability and hemolysis (hemolytic anemia occurs, which is related to hereditary enzymopathies).

Diagram showing the origin and maintenance of blood sugar

4. Diabetes

Diabetes mellitus (DM) is a group of metabolic (metabolic) diseases characterized by the development of persistent hyperglycemia due to absolute or relative insulin deficiency. Lack of insulin and prolonged hyperglycemia cause deviations of all types of metabolic processes with the development of acute and chronic (late) specific complications of diabetes.

With absolute insufficiency of insulin, the concentration in the blood of this hormone is less than normal.

With a relative insufficiency of insulin, its concentration in the blood can be not only normal, but even increased, and the weakening of the effects of insulin is associated with a decrease in sensitivity to it (the development of insulin resistance) on the part of insulin-dependent tissues.

Sugar classification wow diabetes

1. Type 1 diabetes (old name: insulin-dependent diabetes mellitus):

- autoimmune; - idiopathic.

2. Type 2 diabetes (old name: insulin-independent diabetes mellitus)

3. Other specific types of diabetes mellitus:

A. Genetic defectsin-cell function:

a) juvenile MODY-diabetes (in the classification of 1999 there were 3 types, in 2005 - 6 types);

b) mitochondrial DNA mutation;

c) other genetic defects in B-cell function

B. Genetic defects in the action of insulin (mediatedereceptor function):

Insulin resistance type A; - leprechaunism;

Rabson-Mendenhall syndrome; - lipoatrophic diabetes

Other variants of genetic abnormalities of insulin receptors.

C. Diseases of the exocrine pancreas:

Chronic and recurrent pancreatitis, neoplasias, pancreoectomy, cystic fibrosis, fibrocalculous pancreatopathy, hemochromatosis;

G. Endocrinopathy:

Acromegaly, Cushing's syndrome, glucagonoma, pheochromocytoma, thyrotoxicosis, somatostatinoma, aldosteroma, etc.

D. Drug and Chemical Induced Diabetes:

vacor, cyclosporine, pentamidine, nicotinic acid, diazoxide, b-adrenergic agonists, b-blockers, thiazide diuretics, dilantin, b-interferon, glucocorticoids, thyroid hormones, etc.

E. Infections likely to be acutely involved in inflammatory processesinpancreas and subsequent destructionin-cells:

Congenital rubella, mumps, infections caused by cytomegalovirus, coxsackie viruses, etc.

G. Unusual forms of immune-mediated diabetes:

Immobility syndrome, autoantibodies to insulin receptors, etc.

H. Genetic syndromes sometimes associated with diabetes:

Syndromes of Down, Kleinfelter, Shereshevsky-Turner, Wolfram, Lawrence-Moon-Biedl, Prader-Willi, Friedreich's ataxia, Guttington's chorea, myotonic dystrophy, porphyria, etc.

4. Gestational diabetes mellitus.

The pathogenesis of insulin deficiency in diabetes mellitus and na 1.

The leading link in the pathogenesis of T1DM isdestructionin-cells pancreas and, as a result, absolute insulin deficiencyhness. Clinically overt (overt) diabetes occurs when 85-90% of B cells are destroyed. According to the mechanism of triggering islet cell death, T1DM is divided into idiopathic and autoimmune, which occurs 10 times more often than the first.

Autoimmune type 1 diabetes.

The autoimmune form of T1DM is associated with internal (genetic) and external (provoking) factors, which in combination with each other "trigger" immune responses to damage to the islet apparatus.

The likelihood of autoimmune type 1 diabetes is due to certain types and combinations of genes of the HLA system located on chromosome 6 (diabetogenic alleles from the HLA-DP, -DQ, -DR groups), as well as other diabetogenic genes, of which today there are no less than 20 and which are located both on different chromosomes and in different parts of the same chromosome. For example, according to the most recent data, in addition to the genes of the HLA system (chromosome 6), the insulin gene (chromosome 11) is involved in the inheritance of a predisposition to autoimmune type 1 diabetes; a gene encoding an IgG heavy chain (chromosome 14); gene in-chain of the T-cell receptor (chromosome 7); genes of tumor necrosis factors and other cytokines (polychromosomal mosaic localization).

The etiology of autoimmune type 1 diabetes has not been fully established. According to modern concepts, the pathogenetic mechanism of destruction of β-cells in this form of diabetes mellitus can be represented as a sequence of interaction of a significant number of external initiating factors. In individuals genetically predisposed to autoimmune type 1 diabetes, the activation of immunocompetent cells occurs against the background of increased production of various cytokines (interleukin-1, tumor necrosis factor, g-interferon, etc.), pro-inflammatory prostaglandins, nitric oxide, etc., the combined action of which leads to destruction, apoptosis and a decrease in the number of β-cells and the clinical picture of diabetes. It is believed that among the initiating agents the viruses of congenital rubella, mumps, adenoviruses, and Coxsackie viruses are of the greatest importance for the development of autoimmune type 1 diabetes. In turn, the damaging effect of viruses is manifested to a greater extent against the background of possible previous effects on the B-cell membrane:

a) various chemicals at sub-threshold concentrations;

b) transient abnormalities in cellular metabolism provoked by various exogenous causes (hypoxia, vitamin deficiency, lack of trace elements, in particular Cu 2+ and Zn 2+, etc.);

c) inadequate hormonal regulation, especially during puberty and adrenarch (this is indirectly evidenced by the age at the onset of type 1 diabetes, which in most patients corresponds to puberty).

Infiltration of the islet with lymphocytes (Th1, CTL CD8), NK cells and macrophages (insulitis) is constantly encountered at the earliest stages of the development of autoimmune type 1 diabetes and indicates the participation in the pathological processes of the cellular component of immunity.

Autoantibodies to various B-cell antigens are found in the serum of most patients with autoimmune type 1 diabetes at the preclinical stage and in almost all patients at the early stages of the clinical period. The role of autoantibodies in the pathogenesis of T1DM remains open. Some researchers believe that all types of these autoantibodies appear secondarily in response to the destruction of B cells, i.e. do not take part in the induction or maintenance of cytotoxic reactions. Other authors do not exclude the possibility of destruction of β-cells by complement-binding autoantibodies.

Nevertheless, the appearance of the described antibodies indicates the ongoing process of destruction of β-cells, regardless of the presence or absence of clinical signs of diabetes. Therefore, the detection of antibodies to islet cells makes it possible to diagnose autoimmune T1DM already at the latent stage (during the period of damage to a small% of islet cells that does not affect carbohydrate metabolism).

Several periods can be distinguished in the development of T1DM. I - characterized by the presence of a genetic predisposition. Perhaps a provoking event is an infection or intoxication, which triggers autoimmune destruction of B cells. Lasts from 3-4 to 10-12 years. II - during this period, autoimmune destruction of B cells occurs, but the production of insulin by the remaining cells is quite sufficient. III - the period of "latent diabetes": the level of fasting glucose is still normal, but the sugar curve after glucose loading becomes pathological, which indicates a significant decrease in the number of β-cells. IV - the period of "overt diabetes": destroyed about 90% of B-cells, fasting hyperglycemia and diabetes clinic. The usual age of patients by this time is 20 years. V - terminal diabetes with clinical complications.

Pathogenesis of insulin deficiency in type 2 diabetes mellitus.

The leading link in the pathogenesis of T2DM isinsulin resistance(insufficient sensitivity of insulin-dependent tissues to insulin), accompanied by relative insulin deficiency even against the background of compensatory hyperinsulinemia.

Table 5 shows the clinical and laboratory characteristics of T2DM in comparison with T1DM, which allows us to characterize the differences between these two forms of DM. From the material presented in this table, it can be seen that the genetic predisposition to T2DM plays a greater role than in T1DM. Thus, the incidence of T2DM in 1st degree relatives is 20-40% (versus 5-10% in T1DM), and concordance for T2DM in identical twins reaches 80-90% (versus 30-50% in T1DM). The inheritance of T2DM is polygenic; however, unlike the hereditary predisposition to T1DM, it has no connection with genetic abnormalities in the HLA system.

The main signs of diabetes mellitus types 1 and 2

Prevalence in the population
Age of disease onset	children, young people	over 40 years old
Development of symptoms		gradual (months, years)
0 Physique		more often obesity
Insulin in the blood		normal or elevated
	glucosuria and often acetonuria	Glucosuria
Propensity for ketoacidosis
Islet antibodies
Heredity	Amazed< 10% родственников 1-й линии, конкордантность среди близнецов -30-50%	Affected\u003e 20% of 1st line relatives, concordance among twins 80-90%
Association with HLA
Late complications	predominantly microangiopathy	predominantly macroangiopathy

Today, various explanations are offered for the connection of certain genotype features with the risk of T2DM:

According to the most widespread view, there are genetic mutational defects that cause an increased risk of T2DM, similar to that observed in T1DM, with the difference that for T2DM the number of such candidate genes is much larger. To date, more than 30 genes have been identified that control the functions of β-cells and tissue insulin receptors, which are probably involved in the predisposition to T2DM. At the same time, it is suggested that genes that increase the risk of T2DM exert their influence in cooperation not only with each other, but also with genes involved in the pathogenesis of obesity. There is also evidence of the significance in the pathogenesis of T2DM not only of mutational changes in genes encoding the processes of insulin-dependent regulation of carbohydrate metabolism, but also of abnormalities in genes that determine the functions of glycogen synthetase, adrenergic receptors and glucagon receptor. diabetes carbohydrate digestive glycogenosis

There is also a hypothesis that the genetic component in the etiology of T2DM is not caused by mutations, but by changes in the level of expression of genes encoding insulin secretion, its interaction with insulin receptors in target tissues, as well as processes that determine the functional state of insulin receptors in insulin-dependent tissues.

Whatever the nature of the hereditary predisposition to T2DM, it also requires the impact of non-genetic provoking factors. These include primarily obesity, as well as elderly age, physical inactivity, pregnancy, stress. It is assumed that insulin resistance is caused either by a decrease in the number of insulin receptors not in all, but in certain target tissues (muscles, adipose tissue, liver), or by impaired post-receptor interactions (internalization of the hormone-receptor complex, autophosphorylation of the β-subunit of the receptor, or phosphorylation of other protein substrates intracellular signaling systems) in insulin-dependent tissues.

On the part of the islet apparatus, the response to insulin resistance is a compensatory increase in insulin secretion, which over a certain period of time allows one to overcome the existing insulin resistance and prevent the development of persistent hyperglycemia. However, chronic hyperinsulinemia reduces the number of receptors on target cells (desensitization develops), as a result of which insulin resistance increases. B cells gradually lose their ability to respond to hyperglycemia, i.e. produce an amount of insulin that is insufficient to completely normalize the glucose level, which has a constant tendency to increase due to the existing (and at the same time, increasing) insulin resistance. This is how a relative insulin deficiency occurs against the background of compensatory hyperinsulinemia. Long-term active compensatory functioning of β-cells is accompanied by their decompensation, as a result of which, in the late stage of T2DM, insulin deficiency changes from relative to absolute, which dictates the need for insulin therapy (as in T1DM).

5. The nature of metabolic disorders in diabetes mellitus

Carbohydrate metabolism. Due to the absolute or relative deficiency of insulin, the supply of glucose to insulin-dependent tissues (muscle, adipose) decreases, which is accompanied by their energy starvation.

To counteract tissue energy deficiency in the body, processes are activated to increase the level of glucose in the blood:

one). The secretion of glucagon increases, which blocks the hypoglycemic effect of insulin. With pronounced ketoacidosis, corresponding to the maximum tension of carbohydrate metabolism, the secretion of other counterinsular hormones - catecholamines, cortisol and growth hormone - also increases.

2) In the liver and muscles, synthesis is weakened and the breakdown of glycogen is activated.

3) In the intestine, the activity of glucose-6-phosphatase increases, which is accompanied by an increase in the absorption of food glucose into the blood;

4) Gluconeogenesis is enhanced in the liver and, to a lesser extent, in the kidneys. This activates the processes of glycogenolysis (in the liver and muscles), proteolysis (mainly in muscles) and lipolysis (in adipose tissue), which supply substrates for the formation of glucose.

The result of all these changes is hyperglycemia, which provokes both acute and chronic (late) complications of diabetes.

Protein metabolism. The activation of gluconeogenesis in diabetes is accompanied by increased protein breakdown (especially in muscle tissue) and negative nitrogen balance. At the same time, an increase in the levels of urea and amino acids is recorded in the blood and urine.

Excessive protein catabolism hinders the normal course of plastic, including regenerative, processes. This is associated with the fact of poor healing of tissues after their traumatization in patients with diabetes. Deviations in protein metabolism also negatively affect the functioning of the immune system, in particular, the formation of protein mediators and antibodies that regulate the immune response. This explains the weakening of resistance to infection in patients with diabetes. The activation of saprophytic microflora, which causes pustular skin lesions, is facilitated not only by the weakening of local immunity caused by abnormalities in protein metabolism, but also by hyperglycemia itself, which provides favorable substrate conditions for opportunistic microorganisms that actively use glucose. The same disorders contribute to the development of dysbiosis in the urogenital tract and intestines against the background of diabetes mellitus.

Fat metabolism. An increase in lipolysis and inhibition of lipogenesis resulting from a deficiency of insulin and an excess of counterinsular hormones (mainly glucagon) mobilize free fatty acids (FFA) from the depot in adipose tissue. This is accompanied by hyperlipidemia and excessive intake of FFA in the liver, which provokes its fatty infiltration. The liver switches the metabolism of incoming FFAs from the re-esterification process to their oxidation in order to maintain energy metabolism in conditions of intracellular glucose deficiency. In this case, a large amount of acetyl-CoA is formed, which, under conditions of inhibition of lipogenesis (due to a deficiency of NADP + and inhibition of the Krebs cycle), is actively converted into ketone bodies (acetoacetic acid, β-hydroxybutyric acid and acetone).

If the increased formation of ketone bodies in the liver (ketogenesis) begins to exceed the body's ability to utilize and excrete them, the result is ketonemia and the associated metabolic acidosis and intoxication. It is this mechanism that underlies one of the most severe acute complications of diabetes - ketoacidotic coma.

In conditions of excess formation of acetoacetic acid, the synthesis of cholesterol, VLDL and LDL is increased, which is one of the components of atherosclerotic vascular lesions in diabetes.

Water-electrolyte and acid-base balance. Hyperglycemia increases plasma osmolality, which causes polyuria (more than 2 liters of urine per day) and polydipsia (thirst, accompanied by the consumption of large amounts of fluids). Polyuria occurs as a result of osmotic diuresis, when the high osmotic pressure of the primary urine due to glucosuria prevents the reabsorption of water in the renal tubules.

Hyperosmolar hypohydration determines the following important factors of pathogenesis - hypovolemia, decreased blood volume and hypoxia.

Hyperketonemia causes ketonuria - acetone appears in the urine. The excretion of excess ketone bodies by the kidneys occurs in the form of sodium and potassium salts, i.e. there is a significant loss of electrolytes.

The uncontrolled production of ketone bodies leads to the depletion of the alkaline reserve spent on their neutralization, which provokes the onset of metabolic acidosis. The shift in pH to the acidic side is also facilitated by the accumulation of lactate due to the activation of glycolysis during hypoxia.

Late complications of diabetes.

Late complications of diabetes include:

macroangiopathy (obliterating atherosclerosis of the aorta, coronary, cerebral and peripheral arteries; diabetic foot syndrome);

microangiopathy (retinopathy, nephropathy);

diabetic neuropathy;

diabetic cataract.

For T1DM, microangiopathy is typical of late complications, while for T2DM, macroangiopathy is typical. The latter is associated with the age factor, because Patients with T2DM are, as a rule, elderly and senile people, who are characterized by a gradual progression of systemic atherosclerosis, which potentiates the effect of chronic hyperglycemia on arterial vessels.

Pathogenesis of macroangiopathies. At the heart of diabetic macrovascular complications is atherosclerosis, the risk of which in diabetes is about 4-5 times higher than in the population. Typical for diabetic macroangiopathy is, first of all, damage to the vessels of the arterial network of the brain, heart and extremities (especially the lower leg and foot).

The reasons for the increased incidence of systemic atherosclerosis and thrombotic complications in patients with diabetes:

Lipid metabolism disorders are manifested in diabetes mellitus in the form of general lipemia with an increase in VLDL, LDL and a simultaneous decrease in the HDL fraction. This leads to both an increase in lipid deposition in the intima of the arteries, and to rheological disorders (increased blood viscosity), which contribute to thrombus formation.

Endothelial dysfunction. In patients with diabetes, the formation of nitric oxide is reduced, which contributes to a constant increase in vascular tone and a more active formation of adhesion molecules (ICAM-1, E-selectins). Increased adhesion to the endothelium of platelets, macrophages and monocytes promotes the release of biologically active substances from them, provoking local inflammation and thrombus formation.

Changes in the hemostatic system. With diabetes, there is a tendency to a decrease in fibrinolytic activity, an increase in many factors of coagulation and vascular-platelet hemostasis.

Proliferation of smooth muscle cells of arteries in diabetes is stimulated by excessive formation of STH, as well as growth factors released from activated platelets and macrophages accumulating in areas of vessels with pronounced endothelial dysfunction.

Oxidative stress. It is a consequence of glucose autooxidation during prolonged hyperglycemia. There are such glyco-oxidized products as protein carbonyls, lipid peroxides, etc., which directly and indirectly damage the vascular wall.

Pathogenesis of microangiopathies, neuropathy and cataracts

Poorly controlled glycemia is the main, although not the unityknown etiological factor of all chronic complications of diabetes. The long-term and uncontrolled effect of glucose on various structures of cells, tissues and organs has received the definition of glucose toxicity. There are several ways to realize the phenomenon of glucose toxicity.

Protein glycation. Glucose is able to interact with protein to form glycated products without the participation of any enzymes. When glucose and protein interact, early products - Schiff bases and fructosamines are first formed, then they pass into stable glycation products. The degree of glycation is highest in long-lived proteins. At the same time, the functions of blood serum proteins, cell membranes, peripheral nerves, collagen, elastin, lens, LDL, hemoglobin. Conformational changes in proteins due to glycation not only disrupt their function, but also provoke the formation of autoantibodies to such proteins, which contributes to their destruction.

The end products of glycation are directly involved in the expression of various genes involved in the development of pathological reactions and morphological structures.

The result of these processes is a variety of pathological conditions, including nephropathy, neuropathy, retinopathy, cardiomyopathy, impaired oxygen transfer by hemoglobin, followed by tissue ischemia.

Accumulation of sorbitol. In hyperglycemia, glucose accumulates in non-insulin dependent tissues (nervous system, retinal pericytes, lens, vessel walls, pancreas), where it enters along a concentration gradient. Under the influence of aldose reductase, glucose is converted into a cyclic alcohol - sorbitol (normally, almost all glucose must be metabolized intracellularly in a hexokinase reaction with the formation of glucose-6-phosphate, which is then used in various metabolic reactions). With the accumulation of sorbitol, an increase in intracellular osmotic pressure is noted, which causes cellular hyperhydration (osmotic edema). In addition, sorbitol is converted to fructose, which more actively than glucose causes glycation of intracellular proteins and thereby disrupts cellular metabolism.

Autooxidation of glucose. In cells (especially endothelium and nervous tissue) highly reactive free radicals are formed.

In the pathogenesis of nephropathy in diabetes, it should be noted a violation of the synthesis and metabolism of glycosaminoglycans involved in the structure and function of the basement membrane of the glomeruli, and in the pathogenesis of retinopathy - neovascularization as a result of increased formation of various growth factors.

Diagnosis of diabetes mellitus.

The clinical picture of "expanded" diabetes consists of typical symptoms and complaints of patients, which include:

thirst with large amounts of fluids (polydipsia); increased daily urine output (polyuria); weight loss (with T1DM) or obesity (with T2DM) against the background of increased appetite (polyphagia) (3 "P").

In addition, diabetes can reveal: fatigue, weakness; itching, furunculosis; urogenital disorders (chronic pyelonephritis, chronic cystitis, in women - symptoms of vaginitis, in men - balanitis, decreased potency); vascular disorders (ischemic heart disease, cerebrovascular accident, peripheral artery disease, trophic ulcers of the foot); peripheral neuropathy (impaired sensitivity, pain, decreased reflexes); signs of nephropathy (proteinuria, renal edema, arterial hypertension); visual impairment (due to progressive diabetic retinopathy).

Any two of the following three laboratory criteria are sufficient to confirm the diagnosis of diabetes mellitus:

fasting plasma glucose more than 7.0 mmol / l;

2 hours after the tolerance test with 75 g of glucose, the plasma glucose level is more than 11 mmol / l.

glucosuria (with polyuria)

6. Metabolic syndrome

Definition of the concept and diagnosis of metabolic syndrome.

Metabolic syndrome is a symptom complex in persons with obesity and the presence of laboratory signs: 1) disorders of carbohydrate metabolism (impaired glucose tolerance, an increase in fasting glucose levels, hyperinsulinemia); 2) disorders of fat metabolism (an increase in blood triglycerides, a decrease in high-density lipoproteins - HDL). Obesity is diagnosed when body mass index (BMI) values \u200b\u200bare\u003e 30.

Pathogenesis of metabolic syndrome.

The central link in the pathogenesis of metabolic syndrome is insulin resistance. Thus, the mechanisms of development of metabolic syndrome and T2DM are essentially identical. The difference between these two pathologies is that in people with metabolic syndrome (without a combination with T2DM) deviations of indicators characterizing fasting blood glucose or when testing glucose tolerance are lower than those values \u200b\u200bat which the presence of diabetes mellitus is confirmed ... This indicates that in metabolic syndrome that is not associated with diabetes mellitus, the degree of insulin-dependent tissue insensitivity to insulin is less pronounced than in type 2 diabetes. Nevertheless, taking into account the steady progression of insulin resistance in metabolic syndrome (in the absence of timely prescribed treatment), the transition of this state to typical T2DM seems natural.

Of particular importance in the development of insulin resistance in metabolic syndrome is given to abdominal (synonyms: visceral, android, central) obesity. It is known that visceral adipose tissue has a low sensitivity to the anti-lipolytic effect of insulin (especially in the postprandial, i.e., after a meal, period), while at the same time high sensitivity to catecholamines. Intensive lipolysis in visceral adipocytes under the influence of nerve (sympathetic) and hormonal (glucocorticoids, androgens, catecholamines) stimuli in individuals with an excess of abdominal adipose tissue leads to the release of larger than normal amounts of free fatty acids (FFA). Abnormally high amounts of FFA interfere with the binding of insulin to hepatocytes, which reduces the extraction (uptake from the blood) and metabolic processing of insulin by the liver and contributes to the development of systemic hyperinsulinemia. At the same time, FFA suppresses the inhibitory effect of insulin on gluconeogenesis, promoting an increase in hepatic glucose production. An excess of FFA in the blood serves as a source of accumulation of triglycerides and products of non-oxidative metabolism of FFA in skeletal muscles, heart muscle. This is the cause of impaired glucose utilization in these tissues, which is actually a manifestation of peripheral insulin resistance, typical for both metabolic syndrome and T2DM.

Clinical relevance and principles of therapy metabolic si n droma.

The clinical significance of metabolic syndrome is that it can be regarded as a pre-disease for T2DM. In addition, regardless of whether or not this syndrome is combined with diabetes mellitus, metabolic syndrome is an independent risk factor for the development of systemic atherosclerosis and its organ manifestations (coronary heart disease, arterialof hypertension, nephrosclerosis).

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