Animal Models of Polycystic Ovary Syndrome: A Focused Review of Rodent Models in Relationship to Clinical Phenotypes and Cardiometabolic Risk

Capsule:
This is a review of current rodent models used to investigate PCOS, including steroid-induced, pre- and postnatal, and genetic spontaneous models, in relationship to cardiometabolic risk factors, and the potential use of these models in understanding the etiology of cardiovascular disease in PCOS.

Authors:
Danni Shi, M.Sc. and Donna F. Vine, Ph.D.
Volume 98, Issue 1 , Pages 185-193.e2, July 2012

Objective:
To review rodent animal models of polycystic ovary syndrome (PCOS), with a focus on those associated with the metabolic syndrome and cardiovascular disease risk factors.

Design:
Review.

Animal(s):
Rodent models of PCOS.

Intervention(s):
Description and comparison of animal models.

Main Outcome Measure(s):
Comparison of animal models to clinical phenotypes of PCOS.

Result(s):
Animals used to study PCOS include rodents, mice, rhesus monkeys, and ewes. Major methods to induce PCOS in these models include subcutaneous injection or implantation of androgens, estrogens, antiprogesterone, letrozole, prenatal exposure to excess androgens, and exposure to constant light. In addition, transgenic mice models and spontaneous PCOS-like rodent models have also been developed.

Conclusion(s):
Rodents are the most economical and widely used animals to study PCOS and ovarian dysfunction. The model chosen to study the development of PCOS and other metabolic parameters remains dependent on the specific etiologic hypotheses being investigated. Rodent models have been shown to demonstrate changes in insulin metabolism, with or without induction of hyperandrogenemia, and limited studies have investigated cardiometabolic risk factors for type 2 diabetes and cardiovascular disease. Given the clinical heterogeneity of PCOS, the utilization of different animal models may be the best approach to further our understanding of the pathophysiologic mechanisms associated with the early etiology of PCOS and cardiometabolic risk.

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