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Research Article Free access | 10.1172/JCI2081

Androgens stimulate early stages of follicular growth in the primate ovary.

K A Vendola, J Zhou, O O Adesanya, S J Weil, and C A Bondy

Developmental Endocrinology Branch, National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Vendola, K. in: PubMed | Google Scholar

Developmental Endocrinology Branch, National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Zhou, J. in: PubMed | Google Scholar

Developmental Endocrinology Branch, National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Adesanya, O. in: PubMed | Google Scholar

Developmental Endocrinology Branch, National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Weil, S. in: PubMed | Google Scholar

Developmental Endocrinology Branch, National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

Find articles by Bondy, C. in: PubMed | Google Scholar

Published June 15, 1998 - More info

Published in Volume 101, Issue 12 on June 15, 1998
J Clin Invest. 1998;101(12):2622–2629. https://doi.org/10.1172/JCI2081.
© 1998 The American Society for Clinical Investigation
Published June 15, 1998 - Version history
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Abstract

The concept that androgens are atretogenic, derived from murine ovary studies, is difficult to reconcile with the fact that hyperandrogenic women have more developing follicles than normal-cycling women. To evaluate androgen's effects on primate follicular growth and survival, normal-cycling rhesus monkeys were treated with placebo-, testosterone-(T), or dihydrotestosterone-sustained release implants, and ovaries were taken for histological analysis after 3-10 d of treatment. Growing preantral and small antral follicles up to 1 mm in diameter were significantly and progressively increased in number and thecal layer thickness in T-treated monkeys from 3-10 d. Granulosa and thecal cell proliferation, as determined by immunodetection of the Ki67 antigen, were significantly increased in these follicles. Preovulatory follicles (> 1 mm), however, were not increased in number in androgen-treated animals. Follicular atresia was not increased and there were actually significantly fewer apoptotic granulosa cells in the T-treated groups. Dihydrotestosterone treatment had identical effects, indicating that these growth-promoting actions are mediated by the androgen receptor. These findings show that, over the short term at least, androgens are not atretogenic and actually enhance follicular growth and survival in the primate. These new data provide a plausible explanation for the pathogenesis of "polycystic" ovaries in hyperandrogenism.

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