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Genome-wide association of polycystic ovary syndrome implicates alterations in gonadotropin secretion in European ancestry populations

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Hayes, M. Geoffrey, Urbanek, Margrit, Ehrmann, David A., Armstrong, Loren L., Lee, Ji Young, Sisk, Ryan, Karaderi, Tugce, Barber, T. M., McCarthy, Mark I., Franks, Stephen et al.
(2015) Genome-wide association of polycystic ovary syndrome implicates alterations in gonadotropin secretion in European ancestry populations. Nature Communications, 6 . p. 7502. doi:10.1038/ncomms8502

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Official URL: http://dx.doi.org/10.1038/ncomms8502

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Abstract

Polycystic ovary syndrome (PCOS) is a common, highly heritable complex disorder of unknown aetiology characterized by hyperandrogenism, chronic anovulation and defects in glucose homeostasis. Increased luteinizing hormone relative to follicle-stimulating hormone secretion, insulin resistance and developmental exposure to androgens are hypothesized to play a causal role in PCOS. Here we map common genetic susceptibility loci in European ancestry women for the National Institutes of Health PCOS phenotype, which confers the highest risk for metabolic morbidities, as well as reproductive hormone levels. Three loci reach genome-wide significance in the case–control meta-analysis, two novel loci mapping to chr 8p23.1 and chr 11p14.1, and a chr 9q22.32 locus previously found in Chinese PCOS. The same chr 11p14.1 SNP, rs11031006, in the region of the follicle-stimulating hormone B polypeptide (FSHB) gene strongly associates with PCOS diagnosis and luteinizing hormone levels. These findings implicate neuroendocrine changes in disease pathogenesis.

Item Type: Journal Article
Divisions: Faculty of Medicine > Warwick Medical School > Biomedical Sciences
Faculty of Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016)
Faculty of Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine
Faculty of Medicine > Warwick Medical School
Journal or Publication Title: Nature Communications
Publisher: Nature Publishing Group
ISSN: 2041-1723
Official Date: 18 August 2015
Dates:
DateEvent
18 August 2015Published
14 May 2015Accepted
19 November 2014Submitted
Volume: 6
Page Range: p. 7502
DOI: 10.1038/ncomms8502
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Open Access

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