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
Cites
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5 of the 231 references couldn’t be matched to a known paper.
Research works printed but not linked: 8
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“[18] Abbott DH, Barnett DK, Bruns CM, Dumesic DA.”
BackgroundBiochemical Pathways and Modeling
DEANGELIS, A., DeAngelis, L. M., Catherino, W. H., & ROLLENE, N. L. (2020) · Clinical Obstetrics & Gynecology · doi:10.1097/grf.0000000000000583
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Bafrouei, M. H. B., Khazali, H., Kalantar, S. M., & Khoradmehr, A. (2018) · PubMed Central · doi:10.22086/gmj.v0i0.1045
“This can be explained by the fact that these cells are affected by high concentration of LH but not granolusa cells in PCOS subjects [28].”
BackgroundSubbaraj, G. K., & Varghese, S. (2021) · Wiley eBooks · doi:10.1002/9781119654803.ch12
Schleußner, E. (2011) · Springer eBooks · doi:10.1007/978-3-642-12974-2_28
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“Moreover, cumulus cells from women with PCOS were characterized by abnormal expression of many growth factors that are known to play a role in oocyte maturation and developmental competence [21-22].”
BackgroundRole of BMI in PCOS Towards Cardiovascular Risk FactorsPreprint
Arshad, F.-A., Mehmood, R., Kausar, N., Bibi, A., & Khan, M. A. (2020) · Research Square · doi:10.21203/rs.3.rs-52960/v1
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McCartney, C. R., Eagleson, C. A., & Marshall, J. C. (2002) · Informa Healthcare eBooks · doi:10.1201/9780203910948.ch8
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Richards, J. S., & Candelaria, N. R. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21477-6.00060-2
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Liu, W., Tang, T., Feng, J., Wang, C., Lin, L., Wang, S., Zeng, K., Zou, R., Yang, Z., & Zhao, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26679875
Liu, W., Tang, T., Feng, J., Wang, C., Lin, L., Wang, S., Zeng, K., Zou, R., Yang, Z., & Zhao, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26679878
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Liu, W., Tang, T., Feng, J., Wang, C., Lin, L., Wang, S., Zeng, K., Zou, R., Yang, Z., & Zhao, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26679872
Liu, W., Tang, T., Feng, J., Wang, C., Lin, L., Wang, S., Zeng, K., Zou, R., Yang, Z., & Zhao, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26679866
Liu, W., Tang, T., Feng, J., Wang, C., Lin, L., Wang, S., Zeng, K., Zou, R., Yang, Z., & Zhao, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26679884
Liu, W., Tang, T., Feng, J., Wang, C., Lin, L., Wang, S., Zeng, K., Zou, R., Yang, Z., & Zhao, Y. (2024) · Figshare · doi:10.6084/m9.figshare.26679869
Plasticité neuro-structurale de l’hypothalamus dans le syndrome des ovaires polykystiques
Barbotin, A. (2019) · theses.fr (ABES) · doi:10.70675/5c3c5015z53bcz4871zbeeezb7ea08d90009
Mécanismes d'action de l'Œstradiol dans l'ovaire humain en conditions physiologique et polykystique
Marie, C. (2024) · theses.fr (ABES) · doi:10.70675/1310af87z3c5ez4c52zad31z9af8ec853cee
Metabolic aspects of polycystic ovary syndrome
Pappas, D., Kandaraki, E., Kalogirou, A., & Diamanti‐Kandarakis, E. (2026) · Expert Review of Endocrinology & Metabolism · doi:10.1080/17446651.2026.2656240
“Emerging evidence shows that early-life exposure to endocrine disruptors alters DNA methylation and histone landscapes in reproductive and metabolic tissues, with some epigenetic imprints persisting into adulthood and potentially across generations [122–124].”
Kinderwunsch bei polyzystischem Ovarialsyndrom und Adipositas
Bralo, H., Mahner, S., & Rogenhofer, N. N. (2026) · gynäkologie + geburtshilfe · doi:10.1007/s15013-026-6387-x
“…Modelle, dass eine gezielte fetale Androgenexposition bei weiblichen Nachkommen einen Phänotyp induzieren kann, der die zentralen klinischen und endokrinologischen Charak-teristika des PCOS widerspiegelt, einschließlich Hyperandro-genismus und anovulatorischer Dysfunktion [7, 9].”
Javed, M., Suramya, S., Javed, H., & Raisuddin, S. (2026) · Reproductive Sciences · doi:10.1007/s43032-026-02140-5
“This process creates the characteristic cyst-like appearance along the ovarian periphery [44].”
Rose, L., & Kauffman, A. S. (2026) · Journal of Neuroendocrinology · doi:10.1111/jne.70267
Polycystic Ovary Syndrome in the Peripubertal Period
Witchel, S. F. (2007) · Humana Press eBooks · doi:10.1007/978-1-59745-499-5_13
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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