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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