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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Jul 10, 2015; 6(7): 936-942
Published online Jul 10, 2015. doi: 10.4239/wjd.v6.i7.936
Fetal programming of polycystic ovary syndrome
Esra Bahar Gur, Muammer Karadeniz, Guluzar Arzu Turan
Esra Bahar Gur, Guluzar Arzu Turan, Department of Obstetrics and Gynecology, Sifa University Faculty of Medicine, Izmir 35100, Turkey
Muammer Karadeniz, Department of Endocrinology, Faculty of Medicine, Sifa University, Bornova 35100, Turkey
Author contributions: Gur EB, Karadeniz M and Turan GA contributed to this paper.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Muammer Karadeniz, MD, Department of Endocrinology, Faculty of Medicine, Sifa University, Sanayi St. No. 7, Bornova 35100, Turkey. muammermd@hotmail.com
Telephone: +90-232-3434445 Fax: +90-232-3435656
Received: October 20, 2014
Peer-review started: October 21, 2014
First decision: January 20, 2015
Revised: February 23, 2015
Accepted: March 30, 2015
Article in press: April 2, 2015
Published online: July 10, 2015
Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women. Experimental research and clinical observations suggest that PCOS may originate in the very early stages of development, possibly even during intrauterine life. This suggests that PCOS is either genetically-transmitted or is due to epigenetic alterations that develop in the intrauterine microenvironment. Although familial cases support the role of genetic factors, no specific genetic pattern has been defined in PCOS. Several candidate genes have been implicated in its pathogenesis, but none can specifically be implicated in PCOS development. Hypotheses based on the impact of the intrauterine environment on PCOS development can be grouped into two categories. The first is the “thrifty” phenotype hypothesis, which states that intrauterine nutritional restriction in fetuses causes decreased insulin secretion and, as a compensatory mechanism, insulin resistance. Additionally, an impaired nutritional environment can affect the methylation of some specific genes, which can also trigger PCOS. The second hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues, causing the PCOS phenotype to develop in adult life. This review aimed to examine the role of fetal programming in development of PCOS.

Keywords: Polycystic ovary syndrome, Androgens, Fetal programming, Intrauterine growth retardation, Genetic

Core tip: Polycystic ovary syndrome (PCOS) is a highly complex and heterogeneous disorder that is significantly influenced by genetic and environmental factors. There is some evidence that the development of PCOS may begin during the intrauterine period. Fetuses exposed to intrauterine nutritional restriction often have lowered insulin secretion and, as a compensatory mechanism, insulin resistance, which is known as the “thrifty” phenotype. Additionally, an impaired intrauterine nutritional environment can affect the methylation of some specific genes, which can trigger PCOS. The other hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues, causing the PCOS phenotype and related disorders to develop in adult life.