Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 373, Issue 1-2, Pages 21-28Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2013.01.013
Keywords
Fetal programming; Epigenome; Monkey; Metabolic syndrome; Androgen excess
Categories
Funding
- National Institutes of Health [R01-RR013635, R01-DK079888, U01-HD044650, P50-HD044405, P51-RR000167, P51-RR000169, T32-DK07786, M01-RR000425]
- Research Facilities Improvement Program [RR-015459-01, RR-020141-01]
- Winnick Clinical Scholars Award
- Endocrine Fellows Foundation Award
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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. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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