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This version published online on March 7, 2006
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-2757
A more recent version of this article appeared on May 1, 2006
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Submitted on December 19, 2005
Accepted on February 23, 2006

Fetal Programming of Polycystic Ovary Syndrome by Androgen Excess: Evidence from Experimental, Clinical and Genetic Association Studies

Nectaria Xita and Agathocles Tsatsoulis*

Department of Endocrinology, University of Ioannina, Ioannina 45110, Greece

* To whom correspondence should be addressed. E-mail: atsatsou{at}cc.uoi.gr.

Context: Polycystic ovary syndrome (PCOS) is a common endocrine disorder of premenopausal women, characterized by hyperandrogenism, polycystic ovaries and chronic anovulation along with insulin resistance and abdominal obesity as frequent metabolic traits. Although PCOS manifests clinically during adolescence, emerging data suggest that the natural history of PCOS may originate in intrauterine life.

Evidence Acquisition: Evidence from experimental, clinical and genetic research supporting the hypothesis for the fetal origins of PCOS have been analyzed.

Evidence Synthesis: Female primates, exposed in utero to androgen excess, exhibit the phenotypic features of PCOS during adult life. Clinical observations also support a potential fetal origin of PCOS. Women with fetal androgen excess disorders, including congenital 21-hydroxylase deficiency and congenital adrenal virilizing tumors, develop features characteristic of PCOS during adulthood despite the normalization of androgen excess after birth. The potential mechanisms of fetal androgen excess leading to a PCOS phenotype in humans are not clearly understood. However, maternal and/or fetal hyperandrogenism can provide a plausible mechanism for fetal programing of PCOS, and this, in part, may be genetically determined. Thus, genetic association studies have indicated that common polymorphic variants of genes determining androgen activity or genes that influence the availability of androgens to target tissues are associated with PCOS and increased androgen levels. These genomic variants may provide the genetic link to prenatal androgenization in human PCOS.

Conclusion: Prenatal androgenization of the female fetus induced by genetic and environmental factors, or the interaction of both, may program differentiating target tissues toward the development of PCOS phenotype in adult life.
Key words: Fetal programming • polycystic ovary syndrome • genetic polymorphisms




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