Médecine de la Reproduction
MENUPolycystic ovaries syndrome: a genetic, environmental or developmental origin? Volume 20, issue 3, Juillet-Août-Septembre 2018
Figures
- Key words: fetal hyperandrogenism, fetal programing, developmental origin, epigenetics, endocrine disruptors, hyperinsulinism, maternal AMH
- DOI : 10.1684/mte.2018.0714
- Page(s) : 196-205
- Published in: 2018
Polycystic ovary syndrome (PCOS), the most frequent female endocrine disease, affects 7 to 10 % of women of childbearing age, associating ovarian hyperandrogenism with impaired follicular maturation. Insulin resistance although not necessary to the diagnosis, is often present, enhancing thecal hyperandrogenism. Hyperandrogenism and insulin resistance origin includes a genetic component, supported by family aggregation studies and association with genomic variants. However, recently reported epigenetic modifications associated with PCOS, suggest an interaction with environmental factors. The hypothesis of a developmental origin via a deleterious fetal environment (fetal hyperandrogenism, intrauterine growth retardation), and/or exposure to endocrine disruptors) is supported by experimental and epidemiological evidence. Anti Müllerian Hormone (AMH) that remains elevated during pregnancy in case of maternal PCOS, may participate through inhibition of placental aromatase and activation of fetal GnRH neurons, to its trans-generational inheritance, illustrating that PCOS is also a developmental disease.
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License