Journal
FERTILITY AND STERILITY
Volume 77, Issue 1, Pages 167-172Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0015-0282(01)02947-8
Keywords
polycystic ovary syndrome; hyperandrogenism; prenatal androgen excess; rhesus monkey; adrenal hyperandrogenism; DHEAS; testosterone; 17 alpha-hydroxyprogesterone
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Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [P51RR000167, R01RR013635] Funding Source: NIH RePORTER
- NCRR NIH HHS [RR00167, RR13635] Funding Source: Medline
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Objective: To determine whether there is an ovarian thecal cell component to hyperandrogenism exhibited in adult female rhesus monkeys exposed to androgen excess during prenatal life. Design: Prospective nonrandomized study. Setting: An academic research environment. Animal(s): Eleven adult female rhesus monkeys. Intervention(s): Five female rhesus monkeys exposed prenatally to T propionate and six normal females underwent blood sampling immediately before and 24 h after a 200-IU IM injection of recombinant hCG. Main Outcome Measure(s): Serum T, 17alpha-hydroxyprogesterone, DHEAS, and cortisol concentrations determined by RIA. Result(s): Prenatally androgenized females exhibited increased T and 17alpha-hydroxyprogesterone response to recombinant hCG stimulation, compared to control females. Although serum adrenal DHEAS concentrations were elevated in comparison to control females, the increased levels of DHEAS were not dependent on recombinant hCG stimulation. Conclusion(s): Prenatal androgen excess in female rhesus monkeys causes perturbations in ovarian and adrenal steroidogenesis during adulthood, which may both contribute to hyperandrogenism. (Fertil Steril(R) 2002;77:167-72. (C) 2002 by American Society for Reproductive Medicine).
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