Metyrapone-induced corticosterone deficiency impairs glucose oxidation and steroidogenesis in Leydig cells of adult albino rats.

The present study was designed to identify the effects of metyrapone-induced corticosterone deficiency on Leydig cell steroidogenesis in adult male rats. Adult Wistar rats (200-250 g body weight) were treated with metyrapone, an inhibitor of corticosterone synthesis (10 mg/100 g body weight, s.c., twice daily) for 10 days. Experimental animals were killed along with controls, blood was collected, and sera separated for testosterone and estradiol assays. Testes were removed and Leydig cells were isolated, purified and used for estimating the specific activity of 17beta-hydroxysteroid dehydrogenase (17beta-HSD) and 14C-glucose oxidation. Serum testosterone (p < 0.05), Leydig cellular 14C-glucose oxidation (p < 0.001) and the specific activity of 17beta-HSD (p < 0.01) were significantly decreased in metyrapone treated rats. However, serum estradiol was not markedly altered compared to control. In addition to this, a set of in vitro experiments were also performed to identify the effects of metyrapone-induced corticosterone deficiency on hCG and prolactin-induced Leydig cell testosterone production. Metyrapone treatment significantly (p < 0.05) decreased the Leydig cellular basal as well as hCG and its combination with prolactin stimulated testosterone production in vitro. It is concluded from the present study that the inhibitory effects of metyrapone-induced corticosterone deficiency on Leydig cell steroidogenesis are mediated through impaired glucose oxidation and 17beta-HSD activity. In vitro studies showed that corticosterone deficiency impairs not only hCG action but also the potentiating effect of prolactin on Leydig cell steroidogenesis.