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Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities affecting women of reproductive age. While the exact origin of PCOS is unknown, observations from clinical and animal studies suggest that maternal hyperandrogenism may be a contributing factor. Because women with PCOS manifest hyperandrogenism during pregnancy, changes in the gestational endocrine milieu may play a role in the vertical transmission of this syndrome. This review discusses the potential developmental origins of PCOS, the impact of maternal PCOS on the offspring's health and contributions of the postnatal environment, capitalizing on findings from animal models that exhibit a PCOS-like phenotype. In addition, this review highlights the scarcity of data at early gestational stages in humans and the importance of animal experimentation to better understand the cellular and molecular mechanisms involved in the programming of adult diseases, therefore, helping identify therapeutic targets for preventive and treatment strategies. [ABSTRACT FROM AUTHOR]

Abstract: The timing of puberty generally differs between sexes, and this may be due to sex differences in the organization of steroid feedback systems. We propose that the reproductive neuroendocrine default sex is female. If the individual is male, the feedback control of GnRH secretion is programmed early in development, and the pubertal GnRH rise is either advanced or delayed depending upon species. This developmental programming is by androgens. Early programming also reorganizes adult reproductive neuroendocrine function to change a pattern of cyclic gamete release (periodic ovulations) requiring multiple feedback systems to that of a continuous one (spermatogenesis) requiring only the negative feedback control. The multiple feedback systems underlying the complex ovulatory cycle are innate, and in the male the unnecessary feedbacks are abolished or rendered less sensitive during development by the estrogenic, as well as the androgenic metabolites of testosterone. [Copyright &y& Elsevier]