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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Background
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Background
Circulating Irisin and Glucose-Dependent Insulinotropic Peptide Are Associated With the Development of Polycystic Ovary Syndrome
Chang, C. L., Huang, S. Y., Soong, Y. K., Cheng, P. J., Wang, C., & Liang, I. T. (2014) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2014-1180 · Cited by 68
REPRODUCTION SYMPOSIUM: Developmental programming of reproductive and metabolic health1,2
Padmanabhan, V., & Veiga‐Lopez, A. (2014) · Journal of Animal Science · doi:10.2527/jas.2014-7637 · Cited by 63
“Many believe PCOS may be a developmental disorder stemming from in utero exposure to excess androgens (Abbott et al., 2005).”
Polycystic ovarian syndrome – prognosis and outcomes
Hart, R. J., & Norman, R. J. (2006) · Best Practice & Research Clinical Obstetrics & Gynaecology · doi:10.1016/j.bpobgyn.2006.04.006 · Cited by 63
Prenatal Androgen Exposure Leads to Alterations in Gene and Protein Expression in the Ovine Fetal Ovary
Hogg, K., McNeilly, A. S., & Duncan, W. C. (2011) · Endocrinology · doi:10.1210/en.2010-1219 · Cited by 62
“Although this study did not examine the adult ovarian phenotype, prenatal androgen exposure at different time points is associated with changes in adult ovarian function (6, 46).”
Background
Human Fetal Ovary Development Involves the Spatiotemporal Expression of P450c17 Protein
Cole, B., Hensinger, K., Maciel, G. A. R., Chang, R. J., & Erickson, G. F. (2006) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2006-0641 · Cited by 61
Improvement of hyperandrogenism and hyperinsulinemia during pregnancy in women with polycystic ovary syndrome: possible effect in the ovarian follicular mass of their daughters
Crisosto, N., Echiburú, B., Maliqueo, M. A., Pérez, V., de Guevara, A. L., Preisler, J., Sánchez, F., & Sir‐Petermann, T. (2011) · Fertility and Sterility · doi:10.1016/j.fertnstert.2011.10.002 · Cited by 62
Prenatal Exposure to Low Levels of Androgen Accelerates Female Puberty Onset and Reproductive Senescence in Mice
Witham, E. A., Meadows, J. D., Shojaei, S., Kauffman, A. S., & Mellon, P. L. (2012) · Endocrinology · doi:10.1210/en.2012-1283 · Cited by 66
Fetal programming of polycystic ovary syndrome
Gür, E. B. (2015) · World Journal of Diabetes · doi:10.4239/wjd.v6.i7.936 · Cited by 62
Prenatal Testosterone Exposure Alters GABAergic Synaptic Inputs to GnRH and KNDy Neurons in a Sheep Model of Polycystic Ovarian Syndrome
Porter, D. T., Moore, A. M., Cobern, J. A., Padmanabhan, V., Goodman, R. L., Coolen, L. M., & Lehman, M. N. (2019) · Endocrinology · doi:10.1210/en.2019-00137 · Cited by 61
Nonhuman primates as models for human adrenal androgen production: Function and dysfunction
Abbott, D. H., & Bird, I. M. (2008) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-008-9099-8 · Cited by 62
“In adulthood, such androgen excess exposed PA female monkeys exhibit irregular or absent ovulatory menstrual cycles, ovarian hyperandrogenism, enlarged polyfollicular ovaries and luteinizing hormone excess, as well as insulin resistance, increased incidence of type 2 diabetes, visceral adiposity and hyperlipidemia [1,…”
Background
Developmental Programming: Impact of Prenatal Testosterone Excess on Pre- and Postnatal Gonadotropin Regulation in Sheep1
Manikkam, M., Thompson, R. C., Herkimer, C., Welch, K. B., Flak, J. N., Karsch, F. J., & Padmanabhan, V. (2007) · Biology of Reproduction · doi:10.1095/biolreprod.107.063347 · Cited by 61
“Hypersecretion of LH associated with reproductive abnormalities is also evident following prenatal exposure to excess testosterone in female rhesus monkeys [9], mice [10], and rats [11], and it is also seen in women with polycystic ovary syndrome [12, 13].”
BackgroundInfluential
Puberty and polycystic ovary syndrome
Witchel, S. F. (2006) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2006.04.028 · Cited by 61
“LH hypersecretion could reflect a primary intrinsic abnormality of the GnRH pulse generator perhaps related to prenatal programming (Abbott et al, 2005).”
Background
Impaired preadipocyte differentiation into adipocytes in subcutaneous abdominal adipose of PCOS-like female rhesus monkeys
Keller, E., Chazenbalk, G. D., Aguilera, P., Madrigal, V., Grogan, T., Elashoff, D., Dumesic, D. A., & Abbott, D. H. (2014) · Endocrinology · doi:10.1210/en.2014-1050 · Cited by 60
Prenatal Hyperandrogenization Induces Metabolic and Endocrine Alterations Which Depend on the Levels of Testosterone Exposure
Amalfi, S., Vélez, L. M., Heber, M. F., Vighi, S., Ferreira, S. R., Orozco, A. S. V., Pignataro, O. P., & Motta, A. B. (2012) · PLoS ONE · doi:10.1371/journal.pone.0037658 · Cited by 58
“In the brain, a prenatal excess of testosterone induces sex differences [9] and defeminization by increasing pulses of gonadotropin-releasing hormone (GnRH) [13].”
Background
Endocrine and cardiometabolic cord blood characteristics of offspring born to mothers with and without polycystic ovary syndrome
Daan, N. M. P., Koster, M. P. H., Steegers‐Theunissen, R. P. M., Eijkemans, M. J. C., & Fauser, B. C. J. M. (2016) · Fertility and Sterility · doi:10.1016/j.fertnstert.2016.09.042 · Cited by 59
“Intrauterine conditions may potentially contribute to the development of PCOS and associated complications in the later life of exposed offspring (11).”
BackgroundInfluential
Kisspeptin treatment induces gonadotropic responses and rescues ovulation in a subset of preclinical models and women with polycystic ovary syndrome
Romero‐Ruíz, A., Skorupskaite, K., Gaytán, F., Torres, E., Perdices-López, C., Mannaerts, B. M. J. L., Qi, S., León, S., Manfredi-Lozano, M., Lopez-Rodriguez, C., et al. (2019) · Human Reproduction · doi:10.1093/humrep/dez205 · Cited by 59
Inappropriate gonadotropin secretion in polycystic ovary syndrome
Hsu, M.-I., Liou, T., Liang, S.-J., Su, H.-W., Wu, C., & Hsu, C.-S. (2008) · Fertility and Sterility · doi:10.1016/j.fertnstert.2008.01.036 · Cited by 58
“Second, the PCOS risk factor–positive (PCOSrf) group included 74 women who had one and only one of three PCOS components: [1] PCOM only; [2] oligomenorrhea or amenorrhea, or anovulation (Oligo-An) only; [3] and hyperandrogenism and/or hyperandrogenemia (HA) only.”
BackgroundMethodInfluential
The role of sex hormone-binding globulin and androgen receptor gene variants in the development of polycystic ovary syndrome
Xita, N. V., Georgiou, I. A., Lazaros, L. A., Psofaki, V., Kolios, G. C., & Tsatsoulis, A. A. (2008) · Human Reproduction · doi:10.1093/humrep/dem382 · Cited by 58
“In addition, increasing evidence based on experimental animal research supports the developmental origin hypothesis of PCOS, whereby fetal exposure to androgen excess may programme in utero the development of PCOS in adult life (Abbott et al., 2002, 2005; Xita and Tsatsoulis, 2006).”
Background
Associations of Birthweight and Gestational Age with Reproductive and Metabolic Phenotypes in Women with Polycystic Ovarian Syndrome and Their First-Degree Relatives
Legro, R. S., Roller, R. L., Dodson, W. C., Stetter, C. M., Kunselman, A. R., & Dunaif, A. E. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-1849 · Cited by 54
Testosterone-induced downregulation of anti-Müllerian hormone expression in granulosa cells from small bovine follicles
Crisosto, N., Sir‐Petermann, T., Greiner, M., Maliqueo, M. A., Moreno, M. A. C., Aedo, P., & Lara, H. E. (2009) · Endocrine · doi:10.1007/s12020-009-9227-6 · Cited by 55
“It has been hypothesized that the increased number of small follicles present in PCOS is due to the trophic effects of androgens, whether increased locally in the ovary, or systemically, as has been observed in prenatal androgenization experimental models [6, 7 ]. This increased follicular mass, through the secretion…”
Sex differences in the effects of androgens acting in the central nervous system on metabolism
Morford, J. J., & Mauvais‐Jarvis, F. (2016) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2016.18.4/fmauvais · Cited by 53
DNA methylation in polycystic ovary syndrome: Emerging evidence and challenges
Liu, Y., Qin, Y. M., Wu, B., Peng, H., Li, M., Luo, H., & Liu, L. L. (2022) · Reproductive Toxicology · doi:10.1016/j.reprotox.2022.04.010 · Cited by 58
Developmental Programming: Prenatal and Postnatal Androgen Antagonist and Insulin Sensitizer Interventions Prevent Advancement of Puberty and Improve LH Surge Dynamics in Prenatal Testosterone-Treated Sheep
Padmanabhan, V., Veiga‐Lopez, A., Herkimer, C., Salloum, B. A., Moeller, J., Beckett, E. M., & Sreedharan, R. (2015) · Endocrinology · doi:10.1210/en.2015-1235 · Cited by 54
The Pancreas Is Altered by In Utero Androgen Exposure: Implications for Clinical Conditions Such as Polycystic Ovary Syndrome (PCOS)
Rae, M. T., Grace, C., Hogg, K., Wilson, L. M., McHaffie, S. L., Ramaswamy, S., MacCallum, J., Connolly, F., McNeilly, A. S., & Duncan, C. (2013) · PLoS ONE · doi:10.1371/journal.pone.0056263 · Cited by 53
“metabolic aspects, is reminiscent of PCOS in women [4,6,9,10,19].”
BackgroundMethod
Ovarian and Adrenal Hyperandrogenism
Carmina, E. (2006) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1365.011 · Cited by 53
Role of the CAG Repeat Polymorphism of the Androgen Receptor Gene in Polycystic Ovary Syndrome (PCOS)
Schüring, A. N., Welp, A., Gromoll, J., Zitzmann, M., Sonntag, B., Nieschlag, E., Greb, R. R., & Kiesel, L. (2011) · Experimental and Clinical Endocrinology & Diabetes · doi:10.1055/s-0031-1291343 · Cited by 53
Hormone-induced rat model of polycystic ovary syndrome: A systematic review
Noroozzadeh, M., Behboudi‐Gandevani, S., Zadeh–Vakili, A., & Tehrani, F. R. (2017) · Life Sciences · doi:10.1016/j.lfs.2017.10.020 · Cited by 61
“It has been reported that the effect of androgen on the female reproductive system is highly influenced by the time of exposure [8, 39].”
Background
A tale of two steroids: The importance of the androgens DHEA and DHEAS for early neurodevelopment
Greaves, R. F., Wudy, S. A., Badoer, E., Zacharin, M., Hirst, J. J., Quinn, T., & Walker, D. W. (2018) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2018.12.007 · Cited by 54
Non-classic congenital adrenal hyperplasia
Witchel, S. F. (2013) · Steroids · doi:10.1016/j.steroids.2013.04.010 · Cited by 52
Prenatal Exposure to Endocrine Disruptors: A Developmental Etiology for Polycystic Ovary Syndrome
Hewlett, M., Chow, E., Aschengrau, A., & Mahalingaiah, S. (2017) · Reproductive Sciences · doi:10.1177/1933719116654992 · Cited by 61
“Regardless of timing of exposure (early or late), prenatally exposed female rhesus monkeys had ovulatory dysfunction and decreases in menstrual cycle length by 40% to 50% compared to unexposed female monkeys.(17) Another study demonstrated that prenatal excess androgen exposure resulted in increased numbers of small-,…”
Background
Reproductive neuroendocrine dysfunction in polycystic ovary syndrome: Insight from animal models
Roland, A. V., & Moenter, S. M. (2014) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2014.04.002 · Cited by 57
“3.1 Prenatal androgenization recapitulates PCOS phenotypes across species The ability of prenatal androgen to reproduce both reproductive and metabolic traits of PCOS has been demonstrated in rhesus monkeys, sheep, rats, and mice (reviewed in Abbott et al., 2005; Padmanabhan and Veiga-Lopez, 2013).”
BackgroundInfluential
The neuroendocrine genesis of polycystic ovary syndrome: A role for arcuate nucleus GABA neurons
Moore, A. M., & Campbell, R. E. (2015) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2015.10.002 · Cited by 54
A novel method to demonstrate that pregnant women with polycystic ovary syndrome hyper-expose their fetus to androgens as a possible stepping stone for the developmental theory of PCOS. A pilot study
Homburg, R., Gudi, A., Shah, A. M., & Layton, A. (2017) · Reproductive Biology and Endocrinology · doi:10.1186/s12958-017-0282-1 · Cited by 51
“Studies on pregnant monkeys injected with testosterone [2], prevalenceof tom-boy behaviour of female children [3] and even an increased incidence of autism spectrum disorders [4], have all corroborated the possible influence of hyper-exposure to testosterone in-utero.”
Background
A Hyperandrogenic Environment Causes Intrinsic Defects That Are Detrimental to Follicular Dynamics in a PCOS Mouse Model
Bertoldo, M. J., Caldwell, A. S. L., Riepsamen, A. H., Lin, D., Gonzalez, M. B., Robker, R. L., Ledger, W. J., Gilchrist, R. B., Handelsman, D. J., & Walters, K. A. (2019) · Endocrinology · doi:10.1210/en.2018-00966 · Cited by 52
The Time of Prenatal Androgen Exposure Affects Development of Polycystic Ovary Syndrome-Like Phenotype in Adulthood in Female Rats
Tehrani, F. R., Noroozzadeh, M., Zahediasl, S., Piryaei, A., Hashemi, S., & Azizi, F. (2014) · Intern J Endocrinol Metab · doi:10.5812/ijem.16502 · Cited by 50
“Several studies have introduced animal models of PCOS to assess the effects of prenatal exposure of animals to androgen excess; for example in mice, rats, sheep and monkeys, prenatal androgenized animals showed many symptoms of PCOS after puberty such as hyperandrogenemia, increased LH secretion, polycystic ovary, oli…”
BackgroundResultInfluential
Unravelling the epigenetic impact: Oxidative stress and its role in male infertility-associated sperm dysfunction
Sudhakaran, G., Kesavan, D., Kandaswamy, K., Guru, A., & Arockiaraj, J. (2024) · Reproductive Toxicology · doi:10.1016/j.reprotox.2023.108531 · Cited by 53
The New Zealand obese mouse model of obesity insulin resistance and poor breeding performance: evaluation of ovarian structure and function
Radavelli‐Bagatini, S., Blair, A. R., Proietto, J., Spritzer, P. M., & Andrikopoulos, S. (2011) · Journal of Endocrinology · doi:10.1530/joe-11-0022 · Cited by 49
“Perhaps, a better model is the prenatally androgenized rhesus monkey that displays hyperandrogenism, anovulation, polyfollicular and enlarged ovaries and metabolic disturbances including increased adiposity and insulin insensitivity (Abbott et al. 1998, 2005, 2008).”
Background
Pioglitazone improves insulin action and normalizes menstrual cycles in a majority of prenatally androgenized female rhesus monkeys
Zhou, R., Bruns, C. M., Bird, I. M., Kemnitz, J. W., Goodfriend, T. L., Dumesic, D. A., & Abbott, D. H. (2007) · Reproductive Toxicology · doi:10.1016/j.reprotox.2006.12.009 · Cited by 48
Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism
Abruzzese, G. A., Heber, M. F., Ferreira, S. R., Vélez, L. M., Reynoso, R., Pignataro, O. P., & Motta, A. B. (2016) · Journal of Endocrinology · doi:10.1530/joe-15-0471 · Cited by 48
Maternal effects in mammals: Broadening our understanding of offspring programming
Edwards, P. D., Lavergne, S. G., McCaw, L. K., Wijenayake, S., Boonstra, R., McGowan, P. O., & Holmes, M. M. (2021) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2021.100924 · Cited by 49
Why are women with polycystic ovary syndrome obese?
Barber, T. M. (2022) · British Medical Bulletin · doi:10.1093/bmb/ldac007 · Cited by 48
Differential DNA methylation patterns of polycystic ovarian syndrome in whole blood of Chinese women
Li, S., Zhu, D., Duan, H., Ren, A., Glintborg, D., Andersen, M., Skov, V., Thomassen, M., Kruse, T. A., & Tan, Q. (2016) · Oncotarget · doi:10.18632/oncotarget.9327 · Cited by 47
Which origin for polycystic ovaries syndrome: Genetic, environmental or both?
Fénichel, P., Rougier, C., Hiéronimus, S., & Chevalier, N. (2017) · Annales d Endocrinologie · doi:10.1016/j.ando.2017.04.024 · Cited by 50
Birthweight and thinness at birth independently predict symptoms of polycystic ovary syndrome in adulthood
Davies, M. J., March, W. A., Willson, K. J., Giles, L. C., & Moore, V. (2012) · Human Reproduction · doi:10.1093/humrep/des027 · Cited by 46
“As PCOS is a heterogeneous collection of symptoms, different presentations or symptoms may have different underlying aetiologies (Davies and Norman, 2002; Abbott et al., 2005).”
Association Between Vitamin D and Adrenal Parameters with Metabolic and Inflammatory Markers in Polycystic Ovary Syndrome
Maidana, P. N. A., Fritzler, A., Mocarbel, Y., Lana, M. B. P., González, D., Rosales, M., de Chazal, F. G., Sternberg, K., Majek, E. L., Mallea-Gil, S., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-40653-z · Cited by 45
Children born to women with polycystic ovary syndrome—short- and long-term impacts on health and development
Vanky, E., Hanem, L. G. E., & Abbott, D. H. (2019) · Fertility and Sterility · doi:10.1016/j.fertnstert.2019.03.015 · Cited by 44
Evidence-based hormonal, mutational, and endocrine-disrupting chemical-induced zebrafish as an alternative model to study PCOS condition similar to mammalian PCOS model
Sudhakaran, G., Guru, A., Haridevamuthu, B., Murugan, R., Arshad, A., & Arockiaraj, J. (2022) · Life Sciences · doi:10.1016/j.lfs.2021.120276 · Cited by 47

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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