Система Orphus

Symptoms of disease - violation of carbohydrate metabolism

Carbohydrate metabolism and the processes of digestion of carbohydrates in the body; their split with the formation of the intermediate and final products, as well as the formation of compounds, which are not carbohydrates, or the transformation of simple carbohydrates in more complex.

The main role of carbohydrates is determined by their energy function. Blood glucose is a direct source of energy in the body. The rapidity of her decomposition and oxidation, as well as the ability to quickly extract from the depot provide emergency mobilization of energy resources, rapidly rising energy costs in cases of emotional arousal in the intensive muscle loads, etc.

The level of glucose in the blood is 3.3-5.5 mmol/l (60-100 mg%) and is the most important homeostatic constant of the organism. Especially sensitive to a decrease in blood glucose levels (hypoglycemia) is the Central nervous system. A small hypoglycaemia is manifested General weakness and rapid fatigue. Reducing the level of glucose in the blood to 2.2-1.7 mmol/l (40-30% mg) develop convulsions, delirium, loss of consciousness, and autonomic reactions: increased sweating, change the lumen of the skin vessels, etc. This state is called «gipoglikemical coma». Introduction in the blood glucose quickly eliminates these disorders.

Which diseases there is violation of carbohydrate metabolism

Disorders of carbohydrate metabolism

1. Violations of hydrolysis and absorption of carbohydrates

Absorption of carbohydrates is disturbed with the lack of amylolytic enzymes of the gastrointestinal tract (amylase pancreatic juice, etc.). This coming from the food carbohydrates are not split up of sugars and not absorbed. Develops carbohydrate craving.

Absorption of carbohydrates also suffer from the violation of the phosphorylation of glucose in the intestinal wall, emerging with the inflammation of the intestines, with the poisoning of poisons, blocking the enzyme hexokinase (floridzin). Not going the phosphorylation of glucose in the intestinal wall and she did not come to the blood.

Absorption of carbohydrates especially are easily disturbed infants, young children, which have not yet fully formed digestive enzymes and enzymes that ensure the process of phosphorylation and dephosphorylation.

The causes of disorders of carbohydrate metabolism, due to the violation of hydrolysis and absorption of carbohydrates:
- a hypoxia
- violation of the functions of the liver - a violation of the education of glycogen from lactic acid - acidosis (hyperlaccidemia).
- vitamin B1.

2. Violation of the synthesis and the breakdown of glycogen

The synthesis of glycogen can be changed in the direction of the pathological increase or decrease.
The strengthening of the disintegration of glycogen is happening during the excitation of the Central nervous system. Pulses by sympathetic ways go to the depot glycogen (liver, muscles) and activate the glycogenolysis and the mobilization of glycogen. In addition, as a result of excitation of the Central nervous system improves the function of the pituitary gland, the adrenal medulla, thyroid, hormones which stimulate glycogen breakdown.

Increase the disintegration of glycogen in a simultaneous increase in consumption of muscle glucose occurs in severe muscle work.

Decrease in the synthesis of glycogen is happening in inflammatory processes in the liver, hepatitis, in the course of which violated its glycogen is an educational function.

With the lack of glycogen tissue power is switched on fat and protein exchange. Education energy from the oxidation of fat requires a lot of oxygen; otherwise, in excess of the accumulated ketone bodies and the intoxication. The formation of the energy at the expense of proteins leads to loss of the plastic material.

Glycogenosis - disorders of the metabolism of glycogen, followed by a pathological accumulation of glycogen in the bodies.

Gierke disease glycogenosis, due to a congenital lack of glucose-6-phosphatase is an enzyme contained in the cells of the liver and kidneys. Glucose-6-phosphate-for splits off a free glucose from glucose-6-phosphate, which makes it possible transmembrane transition glucose into the cells of these organs in the blood. In case of insufficient glukozo-6-fosfataza glucose lingers inside the cells. Developing hypoglycemia. In kidney and liver accumulates glycogen, which leads to an increase in these bodies. There is a redistribution of glycogen inside the cell in the direction of a significant accumulation of it in the kernel. Increases content in the blood of lactic acid, which strenuously goes glucose-6-phosphate. Develops acidosis. The body suffers from carbohydrate diet.
Sick children, as a rule, die sooner.

Glycogenosis with congenital deficiency of α-glucosidase. This enzyme splits off glucose the remains of the molecules of glycogen and dissolves maltose. It is contained in the lysosomes, and out of touch with phosphorylase cytoplasm. In the absence of α-glucosidase in the lysosomes accumulates glycogen, which pushes the cytoplasm, fills the entire cage and destroys it. The contents of glucose in the blood is normal. Glycogen stored in the liver, kidneys and heart. Metabolism in the myocardium is violated, the heart grows in size. Sick children die early from heart failure.

3. Violations of intermediate metabolism of carbohydrates

To a violation of the intermediate metabolism of carbohydrates may lead to:

1. Gipoksicskie status (for example, with the lack of breathing or circulation, with anemia, etc.), anaerobic phase conversion of carbohydrates prevails over the aerobic phase. Is excessive accumulation in the tissues and blood of lactic and pyruvic acids. The content of lactic acid in the blood increases in several times. Occurs acidosis. Violated enzymatic processes. Reduced education ATF.

2. Disorders of the liver, where in a normal part of lactic acid re-synthesized into glucose and glycogen. When the lesion of the liver this resynthesis of violated. Develop hyperlaccidemia and acidosis.

3. Vitamin B1. Violated the oxidation of pyruvic acid, so as vitamin B1 is included in the kofermenta involved in this process. Pyruvic acid accumulates in excess and partially transformed into lactic acid, the content of which is also increasing. In violation of oxidation of pyruvic acid reduced the synthesis of acetylcholine and disrupted the transmission of nerve impulses. Decreases the formation of pyruvic acid acetyl coenzyme. Pyruvic acid is a pharmacological poison to nerve endings. With the increase in its concentration in 2-3 times there are infringements of sensitivity, neuritis, paralysis, etc.

When gipovitaminose B1 is also violated by and pentose phosphate way the metabolism of carbohydrates, in particular the formation of ribose.

4. Hyperglycemia

Hyperglycemia - increase blood sugar level higher than normal. Depending on the causative factors distinguish the following types of hyperglycemia:

1. Nutritional hyperglycemia. Develops when receiving large amounts of sugar. This type of hyperglycemia use to assess the status of carbohydrate metabolism (the so-called sugar load). In a healthy person after simultaneous reception of 100-150 grams of sugar glucose in the blood increases, reaching a maximum of 1.5-1.7 g/l (150-170 mg%) after 30-45 min. Then the blood sugar level begins to fall and after 2 h decreases to normal (0,8-1,2 g/l), and after 3 hours is even a slight reduction.

2. Emotional hyperglycemia. With a sharp prevalence in the cerebral cortex of the excitatory process over the brake excitement changes on downstream departments of the Central nervous system. The flow of sympathetic impulses to the path, heading to the liver, increases in the demise of glycogen, inhibits the transition of carbohydrates into fat. At the same time the excitement of acts through the hypothalamic centres and the sympathetic nervous system on the adrenal glands. Are released into the blood of large amounts of adrenaline, stimulating glycogenolysis.

3. Hormonal hyperglycemia. Arise in violation of the functions of the endocrine glands and the hormones are involved in regulation of carbohydrate metabolism. For example, hyperglycemia develops with increasing production glukagona - hormone α-cells of the islets of Langerhans of the pancreas, which, by activating phosphorylase the liver, promotes the glycogenolysis. Similar action has adrenaline. To hyperglycemia leads excess of glucocorticoids (stimulate gluconeogenesis and hinder hexokinase) and Somatotropinum pituitary hormone (inhibits the synthesis of glycogen, contributes to the formation inhibitor hexokinase and activates insylinase the liver).

4. Hyperglycemia in some types of anesthesia. When the etheric and morphine anesthesia is an activation of sympathetic centers and output of adrenaline from the adrenal glands; in chloroform anaesthesia join to it the violation of the glycogen educational the functions of the liver.

5. Hyperglycemia with deficiency of insulin is the most persistent and severe. Its reproduce the experiment by removal of the pancreas. However, the deficiency of insulin is combined with severe disorders of the digestive system. Therefore, the more perfect the experimental model of insulin deficiency is a failure caused by the introduction of alloxan (C4H2N2O4), which blocks the SH-groups. In β-cells of the islets of Langerhans of the pancreas, where reserves of SH-groups are small, quickly coming of their deficit and insulin becomes inactive.

Experimental lack of insulin can cause dithizone, blocking zinc in β-cells of the islets of Langerhans, which leads to violation of the formation of granules of molecules of insulin and its Deposit. In addition, in β-cells is formed dithizonate of zinc, which damages the insulin molecules.

Deficiency of insulin may be the pancreatic and out of pancreatic. Both these types of insulin deficiency can cause diabetes (diabetes mellitus).

6. Pancreatic insulin insufficiency

This type of failure develops in the destruction of pancreatic tumors, tuberculosis or syphilitic process, in acute inflammatory-degenerative processes in the pancreas - pancreatitis. In these cases violated all the functions of the pancreas, including the ability to produce insulin. After pancreatitis in 16-18% of cases develop insulin deficiency in connection with an excessive proliferation of connective tissue, which is a kind of «walling up» β-cells, which violates their oxygen supply.

To insulin deficiency leads the local hypoxia of islets of Langerhans (atherosclerosis, spasm of the blood vessels), where the norm is very intensive circulation of the blood. The disulfidnye group in insulin transferred to sulfhydryl and he becomes inactive (does not have hypoglycemic effect).
Assume that the cause of insulin deficiency may serve as an education in the body in violation of purinovogo exchange alloxan that is similar in structure to the uric acid.

The insular apparatus may be depleted after pre-enhancing features, such as when too much eating carbohydrate diet, causing hyperglycemia, overeating.
In the development of pancreatic insulin deficiency important role belongs to the original hereditary inferiority of insulyarnogo apparatus.

7. Out of pancreatic insulin insufficiency

This type of failure can develop with increased activity of the insulinazy - the enzyme that breaks down insulin and formed in the liver by the beginning of puberty.

The deficiency of insulin can cause chronic inflammatory processes, in which the blood receives a lot of proteolytic enzymes that destroy insulin.

The excess of hydrocortisone, inhibitory hexokinase, reduces the action of insulin. Insulin activity decreases with an excess in the blood of nonesterified fatty acids, which influence it in a direct inhibitory effect.

The cause of the deficiency of insulin may be too strong of his connection with transferring proteins in the blood. Insulin associated with the protein, is not active in the liver and muscles, but has generally effect on the fat tissue (the so-called diabetes, obese).

In a number of cases of diabetes mellitus content of insulin in the blood is normal or even increased. Suggest that diabetes is caused by the presence in the blood of the antagonist of insulin, but the nature of this antagonist is not installed.

Education in the body of antibodies against insulin leads to the destruction of this hormone.

Disorders of carbohydrate metabolism in deficiency of insulin.

Carbohydrate metabolism in diabetes mellitus is characterized by the following features:

1. sharply reduced the synthesis of glucokinase, which in diabetes almost completely disappears from the liver, which leads to the reduction of the formation of glucose-6-phosphate in the liver cells. This point, along with reduced synthesis of glycogen synthetase causes a sharp deceleration of glycogen synthesis. Is impoverishment of the liver glycols. With the lack of glucose-6-phosphate is hampered by pentose phosphate cycle;
2. the activity of glucose-6-phosphatase increases dramatically, so glucose-6-phosphate dephosphorylated and enters the blood in the form of glucose;
3. is hampered by the transition of glucose in fat;
4. decreases the flow of glucose across cell membranes, it is poorly absorbed by the tissues;
5. sharply accelerated the gluconeogenesis - the formation of glucose from the lactate, pyruvate, amino acids fatty acids and other products non-carbohydrate exchange. The acceleration of gluconeogenesis in diabetes due to the absence of the overwhelming influence (suppression) of insulin on enzymes, providing gluconeogenesis in the cells of the liver and kidneys: pyruvate carboxylase, glucose-6-phosphatase, etc.

Thus, in diabetes have a place of excess production and insufficient use of glucose tissues, resulting in hyperglycemia occurs. The sugar content in the blood in the worst forms of may reach 4-5 g/l (400-500 mg%) and above. This dramatically increases the osmotic pressure of the blood, which leads to dehydration of the body's cells. In connection with dehydration deeply violated the functions of the Central nervous system (hyperosmolar coma).

Sugar curve with diabetes compared to those from healthy significantly stretched over time. The value of hyperglycemia in the pathogenesis of the disease in two ways. She plays a responsive role, as it is hampered by the disintegration of glycogen and partly increases its synthesis. When hyperglycemia glucose better penetrates the tissues and they do not experience a sharp lack of carbohydrates. Hyperglycemia has a negative value. When it increases the concentration of the gluco - and mukoproteidov, which is easy to fall in the connective tissue, thus contributing into formation of hyaline. So for diabetes characterized by an early defeat of vessels atherosclerosis. Atherosclerotic process captures the coronary vessels of the heart (coronary), vessels of the kidneys (glomerulonephritis) and others.
In the old age, diabetes mellitus can be combined with essential hypertension.

With increasing content of sugar in the blood of up to 1.6-2.0 g/l (160 to 200 mg%) and above, he starts to move into the final urine - there is a glukozuria.

Glukozuria. In normal glucose contained in the provisory the urine. In the bone she reabsorbed in the form of glucose phosphate, for education which is necessary gexokinaza, and after dephosphorylation enters the blood. Thus, in the final urine sugar in normal conditions does not contain. In diabetes, the processes of phosphorylation and dephosphorylation of glucose into the tubules of the kidneys are not able to cope with the excess of glucose in the primary urine. Develops glukozuria. In severe forms of diabetes mellitus content of sugar in the urine can reach 8-10%. The osmotic pressure of urine increased; in connection with this, in the final urine passes a lot of water. Daily diuresis increases of up to 5-10 litres or more (polyuria). Developing dehydration of the body and as a consequence of his - increased thirst (polydypsia).

Which doctor should I contact if there is a violation of carbohydrate metabolism

  • Endocrinologist

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Map of the symptoms and the types of disorders is intended solely for educational purposes. We strongly recommend do NOT self-medicate; on all matters relating to the definition of the disease and ways of its treatment, contact your doctor. Md-tips is not responsible for the consequences of use information posted on the site.