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Development of polycystic ovary syndrome: involvement of genetic and environmental factors.
Int J Androl 2006; 29(1):278-85; discussion 286-90IJ

Abstract

We have recently proposed that polycystic ovary syndrome (PCOS) has its origin in fetal life. This hypothesis is based on data from animal models (rhesus monkey or sheep that have been exposed prenatally to high doses of androgen) and is supported by clinical studies. It is suggested that, in human females, exposure to excess androgen, at any stage from fetal development of the ovary to the onset of puberty, leads to many of the characteristic features of PCOS, including abnormalities of luteinizing hormone secretion and insulin resistance. It is likely that, in humans with PCOS, the development of the PCOS phenotype results primarily from a genetic predisposition for the fetal ovary to hypersecrete androgen. At present, it is unclear whether the maternal environment directly influences the development of PCOS in the offspring. Maternal androgen excess is unlikely to affect the fetus, because the placenta presents an effective barrier, but metabolic disturbances during pregnancy could affect development of the syndrome in the fetus. In postnatal life, the natural history of PCOS can be further modified by factors affecting insulin secretion and/or action, most importantly, nutrition. We now have evidence for a disorder of early follicular development in the polycystic ovary that is consistent with an increased population of primordial follicles in the fetal ovary. It remains to be determined whether this phenomenon is the cause or the effect of increased exposure to androgen within the ovary. PCOS is the commonest endocrine disorder in women. It is not only a very prevalent cause of anovulatory infertility, menstrual disturbances and hirsutism, but it is also a major risk factor for the development of type 2 diabetes mellitus in later life. The aetiology of the syndrome remains uncertain but there is increasing evidence for a genetic basis. PCOS very often becomes clinically manifest during adolescence with maturation of the hypothalamic-pituitary-ovarian axis but the genesis of the syndrome may be during very early development - perhaps even in utero. In this review, this hypothesis is explored in the light of clinical, biochemical and genetic research.

Authors+Show Affiliations

Institute of Reproductive & Developmental Biology, Imperial College London, Hammersmith Hospital, UK. s.franks@imperal.ac.ukNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16390494

Citation

Franks, Stephen, et al. "Development of Polycystic Ovary Syndrome: Involvement of Genetic and Environmental Factors." International Journal of Andrology, vol. 29, no. 1, 2006, pp. 278-85; discussion 286-90.
Franks S, McCarthy MI, Hardy K. Development of polycystic ovary syndrome: involvement of genetic and environmental factors. Int J Androl. 2006;29(1):278-85; discussion 286-90.
Franks, S., McCarthy, M. I., & Hardy, K. (2006). Development of polycystic ovary syndrome: involvement of genetic and environmental factors. International Journal of Andrology, 29(1), pp. 278-85; discussion 286-90.
Franks S, McCarthy MI, Hardy K. Development of Polycystic Ovary Syndrome: Involvement of Genetic and Environmental Factors. Int J Androl. 2006;29(1):278-85; discussion 286-90. PubMed PMID: 16390494.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Development of polycystic ovary syndrome: involvement of genetic and environmental factors. AU - Franks,Stephen, AU - McCarthy,Mark I, AU - Hardy,Kate, Y1 - 2005/12/22/ PY - 2006/1/5/pubmed PY - 2006/4/14/medline PY - 2006/1/5/entrez SP - 278-85; discussion 286-90 JF - International journal of andrology JO - Int. J. Androl. VL - 29 IS - 1 N2 - We have recently proposed that polycystic ovary syndrome (PCOS) has its origin in fetal life. This hypothesis is based on data from animal models (rhesus monkey or sheep that have been exposed prenatally to high doses of androgen) and is supported by clinical studies. It is suggested that, in human females, exposure to excess androgen, at any stage from fetal development of the ovary to the onset of puberty, leads to many of the characteristic features of PCOS, including abnormalities of luteinizing hormone secretion and insulin resistance. It is likely that, in humans with PCOS, the development of the PCOS phenotype results primarily from a genetic predisposition for the fetal ovary to hypersecrete androgen. At present, it is unclear whether the maternal environment directly influences the development of PCOS in the offspring. Maternal androgen excess is unlikely to affect the fetus, because the placenta presents an effective barrier, but metabolic disturbances during pregnancy could affect development of the syndrome in the fetus. In postnatal life, the natural history of PCOS can be further modified by factors affecting insulin secretion and/or action, most importantly, nutrition. We now have evidence for a disorder of early follicular development in the polycystic ovary that is consistent with an increased population of primordial follicles in the fetal ovary. It remains to be determined whether this phenomenon is the cause or the effect of increased exposure to androgen within the ovary. PCOS is the commonest endocrine disorder in women. It is not only a very prevalent cause of anovulatory infertility, menstrual disturbances and hirsutism, but it is also a major risk factor for the development of type 2 diabetes mellitus in later life. The aetiology of the syndrome remains uncertain but there is increasing evidence for a genetic basis. PCOS very often becomes clinically manifest during adolescence with maturation of the hypothalamic-pituitary-ovarian axis but the genesis of the syndrome may be during very early development - perhaps even in utero. In this review, this hypothesis is explored in the light of clinical, biochemical and genetic research. SN - 0105-6263 UR - https://www.unboundmedicine.com/medline/citation/16390494/full_citation L2 - https://doi.org/10.1111/j.1365-2605.2005.00623.x DB - PRIME DP - Unbound Medicine ER -