Nonhuman primate models of polycystic ovary syndrome

David H. Abbott, Lindsey E. Nicol, Jon E. Levine, Ning Xu, Mark O. Goodarzi, Daniel A. Dumesic

Research output: Contribution to journalArticlepeer-review

75 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)21-28
Number of pages8
JournalMolecular and Cellular Endocrinology
Volume373
Issue number1-2
DOIs
StatePublished - Jul 5 2013
Externally publishedYes

Keywords

  • Androgen excess
  • Epigenome
  • Fetal programming
  • Metabolic syndrome
  • Monkey

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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