Semin Reprod Med 2014; 32(03): 183-193
DOI: 10.1055/s-0034-1371090
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Rodent Models of Polycystic Ovary Syndrome: Phenotypic Presentation, Pathophysiology, and the Effects of Different Interventions

Manuel Maliqueo
1   Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
,
Anna Benrick
1   Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
,
Elisabet Stener-Victorin
1   Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
› Author Affiliations
Further Information

Publication History

Publication Date:
08 April 2014 (online)

Abstract

This review focuses on rodent models exposed to sex steroids prepubertally and describes their phenotypes and pathophysiology with specific focus on the estradiol valerate-, dihydrotestosterone-, and letrozole-induced rat polycystic ovary syndrome (PCOS) models. Phenotypic presentations are compared among models as a function of the timing and dose of the exposure. Furthermore, the use of these models to study the possible effects and mechanisms of different treatment modalities relevant for women with PCOS will be discussed. Importantly, we do not claim to review all available rodent models of PCOS. Despite the variety of rodent PCOS models currently available, there is no “gold standard” that mimics the complete range of abnormalities observed in women with PCOS. In this regard, it is important to select the most suitable model for the pathophysiological experiment to be performed or the treatment strategy to be tested. Important variables to take into consideration are dose, route of administration, timing and duration of exposure, and the relevance of the abnormalities of the reproductive and metabolic axes in the rodent model to those observed in human PCOS.

Funding

This study was financed by grants from the Swedish Research Council (Project No. K2012–55X-15276–08–3), The Jane and Dan Olsson Foundations, The Novo Nordisk Foundation, The Hjalmar Svensson Foundation, The Adlerbert Research Foundation, Wilhelm and Martina Lundgrens's Science Fund, and the Swedish federal government under the LUA/ALF agreement (ALFGBG-136481).


 
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