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Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Departments of Pediatrics, Obstetrics and Gynecology, and Environmental Health Sciences, University of Michigan, Ann Arbor, USA.
Fertility & Research Centre, School of Women's and Children's Health, University of New South Wales, Sydney, Australia.
Centre for Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
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2020 (engelsk)Inngår i: Endocrine reviews, ISSN 0163-769X, E-ISSN 1945-7189, Vol. 41, nr 4, artikkel-id bnaa010Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

More than 1 out of 10 women worldwide are diagnosed with polycystic ovary syndrome (PCOS), the leading cause of female reproductive and metabolic dysfunction. Despite its high prevalence, PCOS and its accompanying morbidities are likely underdiagnosed, averaging > 2 years and 3 physicians before women are diagnosed. Although it has been intensively researched, the underlying cause(s) of PCOS have yet to be defined. In order to understand PCOS pathophysiology, its developmental origins, and how to predict and prevent PCOS onset, there is an urgent need for safe and effective markers and treatments. In this review, we detail which animal models are more suitable for contributing to our understanding of the etiology and pathophysiology of PCOS. We summarize and highlight advantages and limitations of hormonal or genetic manipulation of animal models, as well as of naturally occurring PCOS-like females. 

sted, utgiver, år, opplag, sider
Oxford University Press, 2020. Vol. 41, nr 4, artikkel-id bnaa010
Emneord [en]
adipogenic constraint-induced lipotoxicity, androgen excess, developmental programming, genetic manipulation, naturally hyperandrogenic female monkeys, therapeutic prevention
HSV kategori
Forskningsprogram
Translationell medicin TRIM
Identifikatorer
URN: urn:nbn:se:his:diva-18551DOI: 10.1210/endrev/bnaa010ISI: 000545338200003PubMedID: 32310267Scopus ID: 2-s2.0-85086282447OAI: oai:DiVA.org:his-18551DiVA, id: diva2:1445167
Tilgjengelig fra: 2020-06-22 Laget: 2020-06-22 Sist oppdatert: 2020-08-27bibliografisk kontrollert

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