Methyltrienolone influences on the androgen receptors and DNA&RNA synthesis in the liver cells of male rats with alloxan-induced diabetes
Abstract
Introduction: It has been revealed previously, that metabolic imbalances during the diabetes, occurring with multi-organ participation, are accompanied by the decrease of corticosterone concentration in blood and with the depression of DNA & RNA synthesis, and as well as expression of androgen receptors in liver cells.
Aim: The purpose of our study was to examine how exogenous testosterone can correct mentioned liver cell disturbances under the conditions of experimental diabetes.
Methods: The concentrations of glucose, immune-reactive insulin and testosterone were examined in blood in parallel with studying of histology of pancreatic islets - on the 15th, 30th and 45th days from intraperitoneal injection of Alloxan - to confirm the development of adequate model of experimental (alloxan-induced) Diabetes in Wistar Rats aged 2 months and weighting 180-200 g. DNA and RNA synthesis, proliferative activity and androgen receptor expression in the hepatic cells were studied on the same terms of the experiment – to confirm the involvement of liver in diabetes-caused metabolic disturbances. All above-mentioned investigations were repeated in animals undergone to exposure of exogenous synthetic androgen – methyltrienolone during 15 days – beginning from 31st day of Alloxan-induced diabetes.
Results: Methyltrienolone supplementation reduces the alterations of blood concentration of immune-reactive insulin, glucose and testosterone and supports the regeneration of androgen receptors’ expression and DNA/RNA synthesis in hepatocytes. However, the increase of nuclear acids synthesis is accompanied by increase of hepatocytes ploidy but not their proliferation.
Conclusion: The administration of methyltrienolone reduces the effect of “diabetic stress”. Its influence on DNA/RNA synthesis in hepatocytes might be realized through the regeneration of active androgen receptors of liver cells.
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