The role of adrenal androgen secretion, including its regulation and contribution to the total circulating steroid pool in women, is still largely undefined. CONCLUSION: LH/HCG does not have a major role in the regulation of adrenal steroid synthesis in endocrinologically healthy women.Īdrenal glands, HCG, LH, ovary, steroids Introduction
It can be approximated that the ovarian contribution to the circulating levels of 17-OHP, androstenedione and testosterone is 25–30%, and that the adrenals are the primary source of cortisol, DHEA and DHEAS. The basal serum concentrations of these steroids were significantly lower in oophorectomized women (17-OHP 57%, androstenedione 46%, testosterone 25%), and HCG did not increase these levels. In contrast, in group 1, the basal concentrations of serum 17-hydroxyprogesterone (17-OHP), androstenedione, testosterone and estradiol (E 2) were stimulated significantly (17-OHP 105%, androstenedione 31%, testosterone 20%, E 2 136%) by HCG, and the treatment with GnRH agonist decreased the responses. RESULTS: HCG did not stimulate the secretion of cortisol, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulphate (DHEAS) in group 2. METHODS: HCG stimulation tests (a single dose of 5000 IU i.m.) were performed in women at reproductive age (group 1, n = 6, age 21–39 years) before and after treatment with a GnRH agonist for 3 weeks, and in oophorectomized post-menopausal women (group 2, n = 6, 47–59 years) during and after estrogen replacement therapy (ERT). There is evidence that human adrenals express the LH receptor gene and that LH may affect adrenal androgen secretion.
BACKGROUND: The contribution of the adrenal glands to the total circulating steroid pool in women is not well known.
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