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Biomedical subjects

M M Mirakhmedov

Publications and source records attributed to M M Mirakhmedov.

16 recordsLinked to original sources
PubMedDate not supplied

[Tissue metabolism of thyroid hormones in cirrhosis of the liver].

Content and ratio of products of iodothyronine tissue metabolism was studied in liver tissue of rats in normal state and in hepatocirrhosis after administration of 125I-thyroxin. The distinct decrease was observed in accumulation, deiodination and conjugation of thyroxin; the hormone was also converted into triiodothyronine in cirrhotically altered liver tissue. The importance of liver tissue in maintenance of hormonal homeostasis and biological activation of thyroid hormones is discussed.

Animals↗
PubMedDate not supplied

[Causes of development of the diabetic syndrome in patients with diffuse toxic goiter].

Altogether 41 patients with thyrotoxicosis of mean severity at the stage of decompensation were observed. By glucose tolerance they were divided into 3 groups: with normal, flat and disturbed curves. The third group vs. the first group demonstrated higher levels of the thyroid hormones, cortisol and insulin. C-peptide/insulin ratio values were significantly lower than in the first group before and in 120 min. after glucose loading. The second group showed average indices. Evaluation of sensitivity to insulin in 35 patients showed a decreased reaction to insulin in 17 patients, belonging mainly to the third and second groups. The blood levels of thyroxine and cortisol in these 17 patients were raised. The authors have arrived at a conclusion that the development of insulin resistance rather than the disturbed insular apparatus is likely to cause disorders in glucose tolerance in some patients with thyrotoxicosis.

Adult↗
PubMedDate not supplied

[The effect of nerobol and ecdysterone on insulin-dependent processes linked normally and in insulin resistance].

The effect of substances with anabolic activity (metandienone and ecdysterone phytoecdysteroid) on the manifestation of insulin effects was studied on a model of insulin resistance in rats induced by injections of hydrocortisone or by insulin insufficiency caused by alloxan. The sensitivity of the body to i. v. infusion of insulin and the reactivity of isolated fatty tissue to the hormone were increased after administration of these substances to test animals. The above effects of steroids were determined by nonspecific synthesis of total proteins in cells rather than by an increase in insulin secretion.

Adipose Tissue↗
PubMedDate not supplied

[Insulin resistance in experimental hypo- and hyperthyroidism].

The effect of thyroid hormones on the realization of body insulin function was investigated on the models of hypo- and hyperthyroidism. Hyperthyroidism resulting from thyroidectomy, caused the development of insulin resistance, expressed in a lowered body reaction to i. v. insulin infusion, a decrease in tissue sensitivity and reactivity to insulin. Insulin resistance in hypothyroidism was accountable for by a decrease in the serum total activity of insulin-like growth factors. Insulin resistance in hyperthyroidism was less notable and observed only in 10-day administration of thyroiodine; more prolonged administration of the drug (up to 30 days) restored insulin sensitivity. This effect can be accounted for by enhanced insulin independent glucose consumption caused by thyroid hormones.

Adipose Tissue↗
PubMedDate not supplied

[Mechanisms of insulin resistance in pregnancy].

The causes of insulin resistance were studied in rats at late terms of pregnancy. A decrease in the sensitivity to insulin dependent incorporation of glucose in total lipids and CO2 of isolated fatty tissue of pregnant rats was shown. The maximum tissue reaction to insulin (reactivity) did not lessen indicating together with hyperinsulinemia after a glucose tolerance test and a rise of the activity of blood serum insulin-like growth factors the absence of postreceptor defects. An increase in the pregnant rats blood levels of cholesterol, triglycerides and lipoprotein atherogenic fractions was revealed. The latter in physiological concentrations made an inhibitory effect on respiration of liver and thyroid sections of intact rats. Together with the action of hormones of the fetoplacental system it was considered as one of the mechanisms of development of insulin resistance at late terms of pregnancy.

Animals↗
PubMedDate not supplied

[Effects of insulin in vitro in the fatty tissue of rats with alloxan diabetes after insulin treatment or administration of insulin-like growth factors from human serum].

Insulin insufficiency in rats caused by alloxan, results in a decrease in the sensitivity of the fatty tissue to insulin determined by glucose oxidation and synthesis of lipids manifested in a decrease in a maximum response of the tissue to insulin. Multiple injection of insulin as well as of partially purified total fraction of insulinoid growth factors causes an increase in a maximum response of the fatty tissue to insulin and a right-hand shift of dose-response curves. The total effect of the injection of insulin or partially purified growth factors is expressed in elevated sensitivity of the fatty tissue to insulin.

Adipose Tissue↗
PubMedDate not supplied

[Characteristics of disorders of carbohydrate metabolism in rats with stress].

The purpose was to study the effect of stress caused by cavitary operation (the 1st group) and stress resulting from suspending animals at the neck skin fold for 2, 4, 12 and 24 h (the 2nd group) on the development of metabolic diabetic shifts in rats. Postoperative stress was accompanied by a decrease in motor activity of rats and sispension caused intense muscular activity aimed at getting free. All elements of the diabetic syndrome expressed in glucose intolerance, reduction of sensitivity to insulin, reduced insulin action on glucose oxidation in adipose tissue, hyperinsulinemia and a rise of basal glycemia, were revealed in rats with postoperative stress; in rats of the 2nd group they were undetectable. It could be accounted for by muscular activity of animals in these groups.

Animals↗
PubMedDate not supplied

[Causes of hyperinsulinemia and decreased sensitivity to insulin in liver damage].

Chronic contamination of rats with heliotrin causing the development of hepatitis or hepatocirrhosis and partial hepatectomy to decrease the amount of liver cellular elements resulted in intolerance to glucose, a decrease in the sensitivity of the body to insulin, hyperinsulinemia after a glucose-tolerance test. The content of glycogen in the liver of the heliotrin contaminated rats was much lower than that in the controls and after glucose-tolerance an absolute increment of glycogen in the controls was 8.8-fold higher than in the heliotrin-contaminated rats. It was concluded that a decrease in glucose-tolerance and hyperinsulinemia in patients with chronic hepatitis and hepatocirrhosis were determined by a decrease in the amount of functionally active liver cellular elements and the development of insulin resistance.

Animals↗
PubMedDate not supplied

[Mechanism of the increased insulin sensitivity of rats following physical training].

A rise of sensitivity to insulin was noted in healthy rats living an inactive life in a vivarium as a result of regular physical exercises (swimming with load for 30 min. during one month). It was expressed in a drop of glycemia in response to insulin administration in the presence of glycogen load, in greater glucose consumption and glycogen accumulation by tissues during incubation with insulin, in a lesser rise of C-peptide and insulin levels after glycogen load. Muscular activity was shown to incorporate glucose consumption and oxidation mechanisms unrelated to insulin regulation. Physical exercise resulted in a rise of the activity of enzymes involved in oxidation of glucose metabolism intermediate products in the presence of a decrease in the insulin level. A conclusion has been made that physical exercises determine a decrease in a demand for insulin secretion in response to a rise of the glucose level in the blood resulting in decreased insulinemia and consequently in raising sensitivity to insulin.

Animals↗