Prolactin (PRL) binding to Leydig cells in prepubertal and pubertal streptozotocin (STZ)-diabetic and insulin-treated rats was studied. Prepubertal (30-day-old) and pubertal (50-day-old) rats were made diabetic by single injection of STZ (120 and 100 mg/kg b.wt, respectively). After 3 days of STZ administration, a group of rats was given insulin injections subcutaneously (3 U/100 g b.wt/day in 2 equally divided doses). Animals of prepubertal and pubertal groups were killed on postnatal days 51 and 71, respectively. Age-dependent increase in serum testosterone, PRL levels and PRL receptors on Leydig cells were prevented by STZ-diabetes. Insulin administration partly or completely prevented these changes. These results suggest that steroidogenic defects in Leydig cells of prepubertal and pubertal diabetic rats may be associated with decrease in serum PRL levels and its receptors on Leydig cells. Insulin probably has a role in the maintenance of PRL receptor numbers on Leydig cells during pubertal maturation.
The effects of excess corticosterone on luteinizing hormone (LH)-stimulated Leydig cell testosterone production and activity of 11beta-HSD was studied. Adult male rats (200-250 g body weight) were treated with corticosterone-21-acetate (2 mg/100 g body weight, i.m., twice daily) for 15 days. Another set of rats was treated with corticosterone (dose as above) plus LH (ovine LH 100 microg/kg body weight, s.c., daily) for 15 days. Corticosterone administration significantly increased serum and testicular interstitial fluid (TIF) corticosterone but decreased testosterone levels. Administration of LH with corticosterone partially prevented the decrease in serum and TIF testosterone. The oxidative activity of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) was significantly decreased in Leydig cells of rats treated with corticosterone alone and in combination with LH. The direct effect of corticosterone on Leydig cell steroidogenic potency was also studied in vitro. Addition of corticosterone to Leydig cell culture showed a dose dependent effect on LH-stimulated testosterone production. Corticosterone at 50 and 100 ng/ml did not alter LH-stimulated testosterone production, but at high doses (200-400 ng/ml), decreased basal and LH-stimulated testosterone production. Basal and LH-stimulated cAMP production was not altered by corticosterone in vitro. It is concluded from the present study that elevated levels of corticosterone decreased the oxidative activity of 11beta-HSD and thus resulting in impaired Leydig cell steroidogenesis and the inhibitory effects of corticosterone on testosterone production appear to be mediated through inhibition of LH signal transduction at post-cAMP level.
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