Glucose regulation

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Blood glucose is a crucial factor in homeostasis. It is maintained at a certain level of intestines, liver, pancreas, kidney, adrenal gland, adipose tissue, and other organs.

There are several types of carbohydrate metabolism regulation: the substrate, the nervous, renal, hormonal.

Substrate regulation. The main factor determining glucose metabolism, is the level of blood glucose. Border glucose concentration at which the production in the liver is equal to its consumption by peripheral tissues is 5,5-5,8 mmol / l. At a level of less than this, liver supplies glucose to the blood; at higher levels, on the contrary, it dominates glycogen synthesis in the liver and muscles.

Nervous regulation. Stimulation of sympathetic nerves leads to the release of adrenaline from the adrenals, which stimulates breakdown of glycogen in the glycogenolysis process. Therefore, the stimulation of the sympathetic nervous system is observed hyperglycemic effect. Conversely, stimulation of the parasympathetic nerve fibers accompanied by increased release of insulin by the pancreas, glucose enters the cell and hypoglycemic effect.

Renal regulation. In the glomeruli of the kidneys, glucose is filtered and then reabsorbed in the proximal tubules volatile mechanism. The amount of tubular reabsorption is relatively constant with age there is a tendency to decrease. Exceeding the serum level of 8.8 - 9.9 mmol / l of glucose excreted in urine. Glycemic index, in which there is glycosuria, called the renal threshold. On the excretion of glucose in the urine affect glomerular filtration rate, which normally is about 130 ml / min. By reducing the filtering in renal failure or reduction of blood supply to the kidneys, glucose is absent in the urine, even when glucose is significantly higher than the renal threshold, since less glucose is filtered and reabsorbed all she can in the proximal tubules of the kidney. In the case of nephropathy with impaired reabsorption of glucose in the urine may occur even when normoglycemia. Therefore, the level of glucose in the urine can not diagnose diabetes.

Hormonal regulation. On blood glucose level affects a wide range of hormones with virtually only causes insulin hypoglycemic effect. Contrinsular action with increased blood glucose levels have glucagon, adrenaline, glucocorticoids, growth hormone, ACTH, TTT. Effects of insulin and hormones kontrinsulyarnyh normal control fairly stable blood glucose levels. At low concentrations of insulin, in particular during fasting, amplified hyperglycemic effects of other hormones, such as growth hormone, glucocorticoids, epinephrine and glucagon. This occurs even if the concentration of these hormones into the systemic circulation is not increased.

The metabolism of glucose after a meal. Glucose sucked into the intestine to the liver. The liver maintains a constant delivery of energy substrates to other organs, particularly the brain. Glucose uptake in the liver and the brain is not dependent on insulin in muscle and adipose tissue - insulin-dependent. In the first step of all the cells in glucose metabolism - the formation of glucose-6-phosphate. In the liver, insulin stimulates the enzyme glucokinase, converting glucose 6-phosphate into glycogen, an excess of glucose-6-phosphate is converted to fatty acid with subsequent formation of triglycerides, which are released from the liver as very low-density lipoproteins (VLDL). In muscle glucose stored as glycogen enters triglycerides, glucose in the cerebral tissue is used as an energy substrate in adipose tissue.

Physiologically in the regulation of glucose metabolism are the most important two hormones - insulin and glucagon.

Insulin - a polypeptide consists of two chains: the A-chain contains 21 amino acid B-chain - 30 amino acids. Circuit 2 are interconnected by disulfide bonds. Insulin is similar phase in mammalian species: for example, the A-chain is identical in humans, pigs, dogs, sperm whale; B-chain is identical to the bull, goat and pig. In fact, human insulin and porcine differ only in that the carboxyl end of the B-chain is at the amino acid alanine, porcine and human threonine. Therefore, the commercial "human insulin" is produced by replacing alanine to threonine in pig insulin.

Insulin is synthesized as inactive polypeptide chains of the proinsulin, so it is stored in granules of β-cells of pancreatic islets of Langerhans. Activation of proinsulin peptide is a partial proteolysis pas Arg31 and Arg63. As a result, in an equimolar amount produced insulin and C-peptide (connecting peptide).

Insulin in the blood is in free and protein-bound state. Degradation of insulin occurs in the liver (80%), kidney and adipose tissue. C-peptide is also subjected degradation in liver but much slower. The basal concentration of insulin is determined radioimmunologically is healthy 15-20 uU / ml after an oral glucose load level of 1 hour is increased 5-10 times as compared with the original. Fasting insulin secretion rate of 0.5-1 U / hr after ingestion is increased to 2.5-5 U / hr. In healthy people, there are two phases of insulin secretion - early peak (in 3-10 min after glucose load) and peak late (after 20 minutes). Early release of insulin inhibits a sharp rise in glucose levels during its absorption.