摘要
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-transmittedor 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.
Polycystic ovary syndrome （PCOS） is a common endocrinedisorder that affects up to 6.8% of reproductive agewomen. Experimental research and clinical observationssuggest that PCOS may originate in the very early stagesof development, possibly even during intrauterine life.This suggests that PCOS is either genetically-transmittedor is due to epigenetic alterations that develop in theintrauterine microenvironment. Although familial casessupport the role of genetic factors, no specific geneticpattern has been defined in PCOS. Several candidategenes have been implicated in its pathogenesis, butnone can specifically be implicated in PCOS development.Hypotheses based on the impact of the intrauterineenvironment on PCOS development can be groupedinto two categories. The first is the ＂thrifty＂ phenotypehypothesis, which states that intrauterine nutritionalrestriction in fetuses causes decreased insulin secretionand, as a compensatory mechanism, insulin resistance.Additionally, an impaired nutritional environment canaffect the methylation of some specific genes, which canalso trigger PCOS. The second hypothesis postulates thatfetal exposure to excess androgen can induce changesin differentiating tissues, causing the PCOS phenotype todevelop in adult life. This review aimed to examine therole of fetal programming in development of PCOS.
