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

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

Abbott, D.H., Barnett, D.K., Bruns, C.M., Dumesic, D.A.·2005·Human Reproduction Update
DOI 10.1093/humupd/dmi013
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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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Crossref · 10.1093/humupd/dmi013

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5 of the 231 references couldn’t be matched to a known paper.

Research works printed but not linked: 8

  1. Dewailly D, Cortet-Rudelli C and Deroubaix-Allard D (1997) Definition, clinical manifestations, and prevalence of PCOS. In Azziz R, Nestler JE, and Dewailly D (eds) Androgen Excess Disorders in Women. Lippincott-Raven Publishers, Philadelphia, PA, pp 259–268.
  2. Fischer DA (2003) Endocrinology of fetal development. In Larsen PR, Kronenberg HM, Melmed S, and Polonsky KS (eds) Williams Textbook of Endocrinology. 10th edn. WB Saunders, Philadelphia, PA, pp 811–841.
  3. Goy RW and Kemnitz JW (1983) Early, persistent, and delayed effects of virilizing substances delivered transplacentally to female rhesus fetuses. In Zbinden G, Cuomo V, Racagni G, and Weiss B (eds) Application of Behavioral Pharmacology in Toxicology. Raven Press, New York, pp 303–314.
  4. Goy RW, Uno H and Sholl SA (1988) Psychological and anatomical consequences of prenatal exposure to androgens in female rhesus. In Mori T and Nagasawa H (eds) Toxicity of Hormones in Perinatal Life. CRC Press, Inc., Boca Raton, Florida, pp 127–142.
  5. Hoar RM and Monie IW (1981) Comparative development of specific organ systems. In Kimmel CA and Buelke-Sam J (eds) Developmental Toxicology. Raven Press, New York, pp 13–33.
  6. Knobil E and Hotchkiss J (1994) The menstrual cycle and its neuroendocrine control. In Knobil E, Neill J, Ewing LL, Greenwald GS, Markert CL, and Pfaff DW (eds) The Physiology of Reproduction, Vol 2. Raven Press, New York, pp 1971–1994.
  7. Short RV (1974) Sexual differentiation of the brain of the sheep. In Forest MG and Bertrand J (eds) Sexual endocrinology of the perinatal period, Colloque International INSERM, Lyon. INSERM, Paris, France pp. 121–142.
  8. Sperling MA (1994) Carbohydrate metabolism: insulin and glucagons. In Tulchinsky D and Little AB (eds) Maternal–Fetal Endocrinology. 2nd edn. WB Saunders, Philadelphia, PA, pp 380–400.

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Metadata

Authors
Abbott, D. H., Barnett, D. K., Bruns, C. M., & Dumesic, D. A.
Corresponding author
Abbott, D.H.
ORCID
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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