DIABETES (diabetes, Greek diabetes from diabaino to pass through) — patol, the state which is characterized by allocation of large amounts of urine and some chemicals which are formed in an organism in the course of a metabolism. The term «diabetes» was for the first time applied grech, the doctor Aretey Cappadocian (81 — 138) which wanted to emphasize with this name that at patients with this disease the liquid accepted inside does not remain in a body, and «passes through it», being allocated in large numbers with urine. In the description of a disease left by this doctor there are both sugar D.'s signs, and not sugar. The term «diabetes» is included into the name of a number of diseases, neither etiologically, nor pathogenetic not connected among themselves at which water or other chemical substances are emitted with urine in large numbers.
Among patol, states at which, as well as at sugar D., the hyperglycemia and a glycosuria is found distinguish diabetes steroid (see), connected with action of excess quantity of glucocorticoids on exchange of carbohydrates, diabetes pituitary, caused by defeat of a hypothalamus and a hypophysis and connected preferential with action on carbohydrate metabolism of somatotropic and adrenocorticotropic hormones, diabetes thyrogenic, caused by effect of iodinated thyroid hormones, and diabetes adrenalinic.
Pituitary D. can arise at acromegalias (see), thyrogenic — at craw diffusion toxic (see), adrenalinic — at to a pheochromocytoma (see). At a long current all these forms D. can come to the end with defeat of pancreatic islands (Langergans), i.e. pass in sugar D. Znachitelno meet bronze D. less often, or hemochromatosis (see), and also patol, the states connected with excess release of nitrogen — azoturichesky D., or phosphorus — phosphatic. At these forms neither plentiful urination, nor allocation with urine of sugar is noted (see the table).
Diabetes experimental — model of the disease which is artificially caused in animals for studying of an etiology, a pathogeny, exchange disturbances and treatment. It is for the first time created by J. Mehring and O. Minkowski in 1889 by total removal of a pancreas at dogs. These experiences revealed value of defeat pancreas (see) in emergence sugar D. Zatem began to apply the partial pancreatectomy which was leading to sugar D. of easy degree and switching off completely enzymatic activity of a pancreas. For strengthening of symptoms of sugar D. an animal with partially remote pancreas entered glucose or kontrinsulyarny hormones. In 1930 B. Usse and sotr. caused pituitary D. introduction animal extract of a front share of a hypophysis. Further this form of experimental D. was caused introduction of a growth hormone. In 1943 Dunn, Shikhen and IAC-Letchi (J. S. Dunn, H. L. Sheehan, N. G. B. McLetchie) for the first time studied alloxanic. Mesoxalyl urea (see) causes a necrosis of basphilic insulotsit of pancreatic islands without clear defeat of an exocrine part of gland. Okamoto (To. Okamoto, 1949) offered for experimental D.'s calling other chemical substance — dithizon, the complex connection forming with zinc (it is known that pancreatic islands contain a large amount of zinc) and causing a necrosis of basphilic insulotsit.
Experimental D.'s model with a hyperglycemia and a glucosuria is reached by creation of the insulinny insufficiency full or partial, or formation of forms of insulin with low hormonal activity or metabolic inactive.
Depending on a look and age of animals, their individual sensitivity, the nature of the carried-out influence the hyperglycemia can be resistant, tranzitorny or disturbances of carbohydrate metabolism come to light only in changes of indicators of glucose loading. The Tranzitorny hyperglycemia and glucosuria which is not connected with insufficiency of the insulyarny device can be caused by impact on c. N of page (a prick to the area of a bottom of the IV ventricle, and also in some other departments of a brain), and an experimental glucosuria — plentiful administration of carbohydrates, transition from feeding by fats to a diet, carbohydrate-rich.
At floridzinovy D. there is only a glucosuria; the sugar content in blood remains normal or at introduction of high doses of a floridzin decreases. Floridzin (C 21 H 24 O 10 ) collects in big concentration in kidneys, slows down phosphorylation of glucose therefore its return absorption in renal tubules becomes impossible and there is a glucosuria. An experimental animal enter floridzin parenterally in a dose 0,25 — 1 g on 1 kg of weight, at long introduction of such quantities or their exceeding removal of glucose with urine leads to reduction of maintenance of a glycogen in a liver therefore the hypoglycemia can develop.
Streptozototsin — an antibiotic; introduction by his animal leads to destructive changes in (beta cells, to the same three phases in change of level of glucose in blood, as well as administration of mesoxalyl urea or dithizon. A diabetogenic dose for rats of 25 — 65 mg/kg. Administration of niacinamide prevents development of streptozototsinovy.
Experimental D. can be caused administration of kontrinsulyarny hormones: somatotropic, adrenocorticotropic, glucocorticoids, adrenaline, a glucagon, thyroxine and triiodothyronine, and also introduction of antibodies to insulin. At a partial pancreatectomy or incomplete destruction of basphilic insulotsit carry out also combined effects — an animal in addition appoint glucose or enter kontrinsulyarny hormones. All kontrinsulyarny hormones strengthen secretion of insulin in the beginning, but at long introduction lead to exhaustion of pancreatic islands and destructive changes in basphilic insulotsita. Each of these hormones possesses a peculiar action on carbohydrate metabolism: most naturally somatotropic hormone — metapituitary D. and glucocorticoids — steroid D. causes experimental D. (see. Diabetes steroid ).
From the chemical substances causing experimental D. most often apply mesoxalyl urea, is slightly more rare — dithizon and is much more rare — dehydroascorbic to - that, streptozototsin; all these substances cause destructive changes in basphilic insulotsita. The Tranzitorny hyperglycemia as a result of decrease in secretion of insulin is caused by derivatives of tiazid (e.g., a dichlothiazide), long administration of diazoxide can lead to a constant hyperglycemia.
Experimental D. can be also caused by introduction to blood an animal of antibodies to insulin. So, in D.'s mice it was caused by administration of serum of a Guinea pig with antibodies to insulin of a mouse. Further such form of experimental D. was received at dogs, pigs, sheep, rabbits, rats and ducks, and entered antibodies to insulin of the same species of animals and antibodies to heterogeneous insulin. In pancreatic islands there were inflammatory changes — insulits, after the termination of introduction of antibodies the sugar content in blood was gradually normalized.
At experimental diabetes questions of a pathophysiology of exchange disturbances, an immunogenicity of insulin, efficiency of new remedies are intensively studied.
Table. Short characteristic of some forms of diabetes
Bibliography: Diabetes, under the editorship of R. Williams, the lane with English, M., 1964; L of e y t of e from S. M. and Laptev H. H. Sketches on a pathophysiology of a metabolism and endocrine system, page 61, M., 1967, bibliogr.; The guide to endocrinology, under the editorship of B. V. Alyoshin, etc., M., 1973, bibliogr.; E with to and I. A N. Fundamentals of physiology of closed glands, M., 1975; Diabetes mellitus, theory and practice, ed. by M. Ellen-berg a. H. Rifkin, N. Y. a. o., 1970; J o s-1 i n E. P. Diabetes mellitus, Philadelphia, 1971.
Century of P. Klyachko; author of the tab. A. G. Mazowiecki.