The DOI matches its Crossref record; 226 of the 231 references it cites were found in a registry or an index.
Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome
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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“Fetal, neonatal, prepubertal, and/or pubertal ovaries may be genetically predisposed to increased androgen secretion [100, 101].”
From Polycystic Ovary Syndrome: Pathophysiology, Presentation, and Treatment With Emphasis on Adolescent Girls (2019) · cites this paper as [101]
Citations
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Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement
Diamanti-Kandarakis, E., Bourguignon, J.-P., Giudice, L. C., Hauser, R., Prins, G. S., Soto, A. M., Zoeller, R. T., & Gore, A. C. (2009) · Endocrine Reviews · doi:10.1210/er.2009-0002 · Cited by 4,585
“PCOS Prenatal exposure to high levels of testosterone results in fetal programming of PCOS traits (60, 61) Increased levels of serum AGEs in women with PCOS and positive correlation between AGE proteins and testosterone levels (64) Rats fed with high vs.”
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Azziz, R., Carmina, E., Chen, Z., Dunaif, A., Laven, J. S. E., Legro, R. S., Lizneva, D., Natterson-Horowtiz, B., Teede, H. J., & Yildiz, B. O. (2016) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2016.57 · Cited by 2,005
Polycystic ovary syndrome: etiology, pathogenesis and diagnosis
Goodarzi, M. O., Dumesic, D. A., Chazenbalk, G., & Azziz, R. (2011) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2010.217 · Cited by 1,488
“Intrauterine environment Epigenetic changes in fetal life are implicated in the developmental origins of PCOS”
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Metadata
- Authors
- Abbott, D. H., Barnett, D. K., Bruns, C. M., & Dumesic, D. A.
- Corresponding author
- Abbott, D.H.
- 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
- 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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