Добавил:
Upload Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
учебное пособие биохимия английский вариант.doc
Скачиваний:
0
Добавлен:
01.05.2025
Размер:
635 Кб
Скачать
☆

Hormones of pancreas

The chemical structure, physiologic effect, regulation of secretion of somatostatin and pancreatic peptide

Somatostatin is formed in D-cells of pancreas. It can be also formed in hypothalamus, gaster, large intestine, thyroid gland, salivary glands. It is peptide consisting of 14 amino acids. It inhibits the formation of c.AMP, supresses the secretion of insulin and glucagon, Growth hormone, somatotropin, thyroid-stimulating hormone, pancreatic enzymes and secretin. Somatostatin deminishes aggregation of thrombocytes, absorption of glucose and amino acids. It inhibits function of gaster and peristalsis of intestine. Hyperglycemia, hyperaminoacidemia, secretin and cholecystokinin stimulate secretion of somatostatin

Pancreatic peptide consists of 36 amino acids.. it supresses contraction of gall bladder and secretion of pancreatic enzymes. The secretion of pancreatic peptide depends on content of proteins in food and level of glucose in blood plasma

The chemical structure, target-cells, mechanism of action, physiologic effects, regulation of secretion of insulin

Insulin is formed in B-cells of pancreas.

The chemical structure: It is unfull value protein consistsing of 51 amino acids (except of Met and Try). Amino acids of insulin are arranged to 2 polypeptide chains (A and B). A-chain consists of 21 amino acids; B-chain does 30 amino acids. These chains are linked by 2 disulfidic bonds. Third disuldidic bond occurs in A-chain. Monomers of Insulin are combined with zinc forming polymer consisting of 2-8 molecules of insulin. Insulin is broken up in liver under action of insulinase.

Mechainism of action: 3-rd one

Receptor of insulin consists of 4 subunits (2 alfa and 2 beta). Subunits are bound by disulfidic bridges. B-chain of insulin joins with alfa-subunits of receptor. Beta-subunits of receptor are catalytic part of receptor (tyrosine-kinase).

Target-cells: all cells of the body except nervous system, lens, erythrocytes. Coupled insulin has receptors in adipose tissue only.

Physiologic action: insulin is anabolic hormone that is stimulates synthesis of glycogen, proteins and lipids. The cleavage of proteins, lipids and glycogen is decreased.

  1. The influence on Carbohydrate Metabolism: 1) increase the permeability of membranes for glucose; 2) increase glycogenogenesis; 3) increase of glycolysis; 4) decrease glycogenolysis

  2. The influence on lipid metabolism: 1) increase of synthesis of lipids (incl FFA, Cholseterol); 2) increase of liponeogenesis from glucose and its intermediaries; 3) increase oxidation of glycerol; 4) decrease beta-oxidation of FFA, ketogenesis

  3. The influence on protein metabolism: 1) increase protein synthesis; 2) decrease protein cleavage

  4. Stimulation of cells division

Regulation of secretion: low level of glucose in blood plasma decreases insulin formation. high level of glucose increases insulin formation

The chemical structure, target-cells, mechanism of action, physiologic effects, regulation of secretion of glucagon

The chemical structure: It is peptide consisting of 29 amino acids. It is formed in A-cells of pancreas. It is also formed in some cells of intestinal mucosa.

Target-cells: are cells of liver, muscles, adipose tissue, myocardium, B-cells of pancreas

Mechanism of action: 1-st through c.AMP

Physiologic effects:

This hormone increases the level of glucose in blood plasma due to gluconeogenesis from lipids (from glycerol). The glycogenolysis and lipolysis are increased too. But effect on glycogenolysis lasts during short time. Therefore gluconeogenesis is a main reason of increase of glucose in blood plasma.

Regulation of secretion high level of glucose decreases glucagon secretion. Low level of glucose in blood plasma increases one.

Biochemical bases of hyper- and hypofunction of pancreas

Hyperfunction of pancreas with regard to insulin is observed in non-malignant tumor of B-cells of pancreas and overdose of insulin. It results in hypoglycemia which expressed by weakness, increased sweating, decreased vision. Emergancy is injection of glucose.

Diabetes mellitus is a lack of insulin or its receptors. There are insulindependent (IDDM) and insulinindependent (IIDM) diabetes mellitus. Diagnosis of diabetes mellitus is based on the level of glucose in blood, glucosuria, ketonemia and ketonuria. If the level of glucose on empty stomach is more than 7.8mM/l so it is diebetes mellitus. If the level of glucose in occasional sample of blood plasma is more than 11.1mM/L so it is also diabetes mellitus.

IDDM is associated with deficiency of insulin. IIDM is associated with lack of receptors or excess of contrinsular hormones.

There are diabetes related with absence of free insulin and presence of coupled one (it is due to the action of coupled insulin on adipose tissue where lipogenesis is increased). Such patients are fatty. But another type of diabetes is associated with absence both of forms of insulin. Such patients are skinny (thin).

There are 3 main symptoms of diabetes mellitus: polyuria, polyphagia and polydypsia. Biochemical analysis show hyperglycemia, glucosuris, ketonemia and ketonuria.

Hyperglycemia is associated with deficiency of insulin and excess of contrinsular hormones because glucose doesn’t enter the cells and isn’t used in them. It results in polyphagia (hunger). High level of glucose causes dehydration of tissues because water exits from cells and enters the vessels to dissolve the blood. If the level of glucose is more than renal threshold of its the glucose passes through kidneys in urine and glucosuria is developed. Glucose draws water therefore polyuria is observed. Polyuria causes polydypsia (thirsty).

High level of glucose in blood plasma causes formation of glycosylated hemoglobin. Such hemoglobin doesn’t carry out its function and hypoxia occurs. It results lactate acidosis.

Excess of contrinsular hormones leads to increased lipolysis and subequent ketogenesis. Ketonemia and ketonuria are developed.

In insulinindependent tissues fructose-sorbitol pathway is activated. It results in lesion of these tissues (micro- and macroangiopathies, cataracts, retinopathy, nephropathy, trophic ulcerus)