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15 February 2012 Rodent Models for Human Polycystic Ovary Syndrome
Kirsty A. Walters, Charles M. Allan, David J. Handelsman
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Polycystic ovary syndrome (PCOS) is the most frequent female endocrine disorder, affecting 5%–10% of women, causing infertility due to dysfunctional follicular maturation and ovulation, distinctive multicystic ovaries and hyperandrogenism, together with metabolic abnormalities including obesity, hyperinsulinism, an increased risk of type 2 diabetes, and cardiovascular disease. The etiology of PCOS is unclear, and decisive clinical studies are limited by ethical and logistic constraints. Consequently treatment is palliative rather than curative and focuses on symptomatic approaches. Hence, a suitable animal model could provide a valuable means with which to study the pathogenesis of the characteristic reproductive and metabolic abnormalities and thereby identify novel and more effective treatments. So far there is no consensus on the best experimental animal model, which should ideally reproduce the key features associated with human PCOS. The prenatally androgenized rhesus monkey displays many characteristics of the human condition, including hyperandrogenism, anovulation, polycystic ovaries, increased adiposity, and insulin insensitivity. However, the high cost of nonhuman primate studies limits the practical utility of these large-animal models. Rodent models, on the other hand, are inexpensive, provide well-characterized and stable genetic backgrounds readily accessible for targeted genetic manipulation, and shorter reproductive life spans and generation times. Recent rodent models display both reproductive and metabolic disturbances associated with human PCOS. This review aimed to evaluate the rodent models reported to identify the advantages and disadvantages of the distinct rodent models used to investigate this complex endocrine disorder.

© 2012 by the Society for the Study of Reproduction, Inc.
Kirsty A. Walters, Charles M. Allan, and David J. Handelsman "Rodent Models for Human Polycystic Ovary Syndrome," Biology of Reproduction 86(5), (15 February 2012).
Received: 15 November 2011; Accepted: 1 February 2012; Published: 15 February 2012

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