Cited by 555Ovarian function and disordersSexual Differentiation and DisordersReproductive Biology and Fertility

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Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome

Abbott, D.H., Barnett, D.K., Bruns, C.M., Dumesic, D.A.·2005·Human Reproduction Update

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Abstract

The aetiology of polycystic ovary syndrome (PCOS) remains unknown. This familial syndrome is prevalent among reproductive-aged women and its inheritance indicates a dominant regulatory gene with incomplete penetrance. However, promising candidate genes have proven unreliable as markers for the PCOS phenotype. This lack of genetic linkage may represent both extreme heterogeneity of PCOS and difficulty in establishing a universally accepted PCOS diagnosis. Nevertheless, hyperandrogenism is one of the most consistently expressed PCOS traits. Animal models that mimic fetal androgen excess may thus provide unique insight into the origins of the PCOS syndrome. Many female mammals exposed to androgen excess in utero or during early post-natal life typically show masculinized and defeminized behaviour, ovulatory dysfunction and virilized genitalia, although behavioural and ovulatory dysfunction can coexist without virilized genitalia based upon the timing of androgen excess. One animal model shows particular relevance to PCOS: the prenatally androgenized female rhesus monkey. Females exposed to androgen excess early in gestation exhibit hyperandrogenism, oligomenorrhoea and enlarged, polyfollicular ovaries, in addition to LH hypersecretion, impaired embryo development, insulin resistance accompanying abdominal obesity, impaired insulin response to glucose and hyperlipidaemia. Female monkeys exposed to androgen excess late in gestation mimic these programmed changes, except for LH and insulin secretion defects. In utero androgen excess may thus variably perturb multiple organ system programming and thereby provide a single, fetal origin for a heterogeneous adult syndrome.

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BackgroundInfluential
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Background
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Authors: Abbott, D. H., Barnett, D. K., Bruns, C. M., & Dumesic, D. A.
Corresponding author: Abbott, D.H.
ORCID: Abbott, D.H.
Dumesic, D.A.
Venue: Human Reproduction Update
Publisher: Oxford University Press (OUP)
Published: 2005-07-01
Volume: 11
Issue: 4
Pages: 357-374
ISSN: 1355-4786 (ISSN-L)
1460-2369
DOI: 10.1093/humupd/dmi013
OpenAlex: W2123009569
Cited by: 555
References: 231
Citations by year: 2026: 9 · 2025: 17 · 2024: 24 · 2023: 27 · 2022: 27 · 2021: 21 · 2020: 27 · 2019: 37 · 2018: 23 · 2017: 30 · 2016: 34 · 2015: 28 · 2014: 32 · 2013: 31 · 2012: 23
FWCI: 4.24
Type: journal article
Language: en
Open access: closed
Locations: Human Reproduction Update (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5u01hd044650-05)
National Institute on Aging (T32AG000268)
National Center for Research Resources (R01RR013635, R21RR014093, P51RR000167)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD044405, U01-HD044650)
Topics: Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Sexual Differentiation and Disorders
Health Sciences › Medicine › Reproductive Medicine › Reproductive Biology and Fertility
Keywords: polycystic ovary syndrome, hyperandrogenism, fetal programming, developmental origins of health and disease, rhesus monkeys, prenatal androgen exposure, ovulatory dysfunction, insulin resistance, hyperlipidemia
MeSH terms: Androgens, Animals, Female, Genitalia, Female, Humans, Polycystic Ovary Syndrome, Hyperandrogenism

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Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome

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