Literature DB >> 10383487

Impact of testosterone and oestradiol on region specificity of skeletal muscle-ATP, creatine phosphokinase and myokinase in male and female Wistar rats.

A Ramamani1, M M Aruldhas, P Govindarajulu.   

Abstract

The main aim of the present study was to test the hypothesis that skeletal muscle ATP concentration, creatine phosphokinase and myokinase enzyme activities are stimulated by the sex steroids in both male and female rats (animals were not subjected to any kind of exercise or any training). To test the hypothesis healthy mature (90-120 days old, weighing about 160-180 g) male and female rats were gonadectomized. Gonadectomized male and female rats were administered with testosterone (Sigma Chemical, St Louis, MO, USA) at a dose of 100 microg (100 g body weight)-1 day-1 for males and 5 microg (100 g body weight)-1 day-1 for females for 30 days from day 31 post-castration onwards; and oestradiol at a dose of 5 microg (100 g body weight)-1 day-1 for 30 days from day 31 post-castration onwards for both males and females (17beta oestradiol, Sigma Chemical Company, St Louis, MO, USA). The ATP content, creatine phosphokinase and myokinase enzyme activities of skeletal muscles were significantly higher than that of skeletal muscles of female control rats. Gonadectomy resulted in a significant decrease in ATP content and creatine phosphokinase myokinase enzyme activities in both male and female rats. Testosterone treatment to gonadectomized male rats brought back the parameters to normalcy whereas the same to the female rats enhanced the enzyme activities and ATP contents to the level of control male rats. Oestradiol treatment to castrated male rats did not bring about any significant alterations whereas the same in gonadectomized female rats brought them back to normalcy. Therefore from the present study it is concluded that testosterone is effective in both males and females whereas oestradiol was effective only in the females in enhancing skeletal muscle energy metabolism.

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Year:  1999        PMID: 10383487     DOI: 10.1046/j.1365-201x.1999.00576.x

Source DB:  PubMed          Journal:  Acta Physiol Scand        ISSN: 0001-6772


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