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Mol Cell Endocrinol. 2013 Jul 5;373(1-2):21-8. doi: 10.1016/j.mce.2013.01.013. Epub 2013 Jan 29.

Nonhuman primate models of polycystic ovary syndrome.

Author information

1
Department of Obstetrics and Gynecology, University of Wisconsin, Madison, WI, USA. abbott@primate.wisc.edu

Abstract

With close genomic and phenotypic similarity to humans, nonhuman primate models provide comprehensive epigenetic mimics of polycystic ovary syndrome (PCOS), suggesting early life targeting for prevention. Fetal exposure to testosterone (T), of all nonhuman primate emulations, provides the closest PCOS-like phenotypes, with early-to-mid gestation T-exposed female rhesus monkeys exhibiting adult reproductive, endocrinological and metabolic dysfunctional traits that are co-pathologies of PCOS. Late gestational T exposure, while inducing adult ovarian hyperandrogenism and menstrual abnormalities, has less dysfunctional metabolic accompaniment. Fetal exposures to dihydrotestosterone (DHT) or diethylstilbestrol (DES) suggest androgenic and estrogenic aspects of fetal programming. Neonatal exposure to T produces no PCOS-like outcome, while continuous T treatment of juvenile females causes precocious weight gain and early menarche (high T), or high LH and weight gain (moderate T). Acute T exposure of adult females generates polyfollicular ovaries, while chronic T exposure induces subtle menstrual irregularities without metabolic dysfunction.

PMID:
23370180
PMCID:
PMC3683573
DOI:
10.1016/j.mce.2013.01.013
[Indexed for MEDLINE]
Free PMC Article
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