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Chapter 7 - Origins of Polycystic Ovary Syndrome In Utero

Published online by Cambridge University Press:  13 May 2022

By
Roy Homburg  and
Claudia Raperport
Edited by
Gabor T. Kovacs ,
Bart Fauser  and
Richard S. Legro
Gabor T. Kovacs
Affiliation:
Monash University, Melbourne, Australia
Bart Fauser
Affiliation:
University Medical Center, Utrecht, Netherlands
Richard S. Legro
Affiliation:
Penn State Medical Center, Hershey, PA, USA
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Summary

Polycystic ovarian syndrome (PCOS) affects up to 18% of women internationally, with widespread effects on their reproductive, metabolic and cardiovascular health. To date, the etiology of this syndrome remains unclear. Patterns of expression within family groups suggest a genetic inheritance but neither a clear inheritance pattern nor candidate gene(s) has been discovered to date. Animal studies have proven that in utero exposure to high levels of androgen can elicit PCOS-like traits in various mammals, including rhesus monkeys who share a similar reproductive biology with humans. An alternate mechanism for etiology is the epigenetic alteration in programming of the fetal ovaries in response to androgen exposure. This chapter summarizes the evidence available and hypothesizes possible mechanisms of action via which PCOS could be transmitted from an affected mother to her offspring. The origins of androgens in the fetal circulation as well as the role of AMH and luteinizing hormone (LH) are discussed as are the actions of the placenta and the difference in placental function and hormone secretion patterns in PCOS females compared to “normal” physiology.

Keywords

polycystic ovarian syndrome (PCOS)epigeneticandrogenin uteroplacentaanti-Müllerian hormone (AMH)familialBarker hypothesis
Type
Chapter
Information
Polycystic Ovary Syndrome , pp. 58 - 66
Publisher: Cambridge University Press
Print publication year: 2022

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