Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 19, Issue 32, Pages 5775-5791Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612811319320012
Keywords
Polycystic ovary syndrome; androgen excess; hyperandrogenism; inflammation; endothelial dysfunction; insulin resistance; abdominal adiposity; obesity
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Funding
- Instituto de Salud Carlos III, Spanish Ministry of Economy and Competitiveness [PI080944, PI1100357]
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Chronic low-grade subclinical inflammation has been increasingly recognized as an interposer in the endocrine, metabolic and reproductive disturbances that characterize the polycystic ovary syndrome (PCOS). Abdominal adiposity and obesity are often present in PCOS. Mounting evidence indicates that adipose tissue is involved in innate and adaptive immune responses. Continuous release of inflammatory mediators such as cytokines, acute phase proteins, and adipokines perpetuates the inflammatory condition associated with obesity in women with PCOS, possibly contributing to insulin resistance and other long-term cardiometabolic risk factors. Genetic variants in the genes encoding inflammation-related mediators underlie the development of PCOS and their interaction with environmental factors may contribute to the heterogeneous clinical phenotype of this syndrome. In the future, strategies ameliorating inflammation may prove useful for the management of PCOS and associated conditions.
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