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hCG‐STIMULATION OF TESTICULAR STEROIDOGENESIS DURING INDUCED HYPER—AND HYPOPROLACTINAEMIA IN MAN
Author(s) -
MARTIKAINEN H.,
VIHKO R.
Publication year - 1982
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1982.tb00711.x
Subject(s) - endocrinology , medicine , hyperprolactinaemia , testosterone (patch) , sulpiride , prolactin , bromocriptine , dihydrotestosterone , pregnenolone , stimulation , androgen , basal (medicine) , androstenedione , chemistry , steroid , dopamine , hormone , dopaminergic , insulin
SUMMARY In order to elucidate the role of prolactin in the regulation of testicular steroidogenesis in man, hyper‐ and hypoprolactinaemia were induced by sulpiride (group 2) and bromocriptine (group 3) administration in eight and nine young adults, respectively, and the responses of testosterone and six other steroids to a single dose of 5000 iu hCG were compared with those obtained under basal conditions (group 1) in eight men. During hyperprolactinaemia (group 2) the responses of pregnenolone, progesterone, 17‐hydroxyprogesterone, testosterone and 5α‐dihydrotestosterone tended to be greater than in the control and hypoprolactinaemia groups, but these changes were not statistically significant. In contrast to the behaviour of these steroids, oestradiol showed diminished peak values at 24–36 h after hCG in the sulpiride‐treated group and the response was significantly smaller ( P < 0·01) than during hypoprolactinaemia. These findings suggest that testicular aromatization is modulated by prolactin and thus the partial inhibition of oestradiol production, observed during short‐term hyperprolactinaemia, may result in a better androgen response to hCG.