Stimulatory Effect of Prolactin on Luteinizing Hormone-Induced Testicular 5α-Reductase Activity in Hypophysectomized Adult Rats*

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Abstract
Two pituitaries from 7-week-old female rats were grafted under the capsule of the left kidney of 50-day-old male rat to induce hyperprolactinemia. All of the pituitary-grafted and sham-operated rats were hypophysectomized at 56 days of age. The hypophysectomized rats in groups of 4 were given daily sc injections of saline or 9 μg NIADDK-ovine-(o)LH-23 for 4 and 5 days starting from days 58 and 70, respectively (short and long term hypophysectomized groups). The metabolism of [3H]progesterone or [14C]androstenedione by testicular homogenates, concentrations of testosterone and 5α-androgens (androsterone plus 5α-androstane-3α,17β-diol) in the serum and testes, and testicular LH receptors were estimated. Hypophysec-tomy caused significant decreases in testicular enzyme activities per gram of tissue, andrpgen production, and testicular LH receptors. In the testes of hypophysectomized rats, LH treatment significantly stimulated 5α-reductase and 17-bydroxylase activities. Although pituitary grafts alone showed little or no effect on these testicular enzyme activities, hyperprolactinemia induced by the grafts markedly enhanced the LH-stimulated 5α-reductase activity in both groups, especially in the long term hypophysectomized group. Therefore, androsterone and 5α-an-drostane-3α,17β-diol were shown to be the major C19-steroid products (immature type of testicular androgen production) in the LH- and PRL-stimulated testes of long term hypophysec-tomized adult rats. On the other hand, hyperprolactinemia was associated with a significant inhibition and a slight increase of the LH-stimulated 17-hydroxylase activities in the short and long term hypophysectomized groups, respectively. This difference can be attributed to both a PRL-induced increase in testicular LH receptors and a PRL-induced inhibition of 17-hydrox-ylase via a postreceptor mechanism(s). The present findings demonstrate for the first time that PRL directly stimulates LH-induced 5α-reductase activity in the testes. It appears that PRL may play a role in the increased production of 5α-C19-steroids and the parallel decrease of testosterone production in immature rat testes. (Endocrinology118: 2268–2275, 1986)