SFEBES2008 Poster Presentations Reproduction (22 abstracts)
Association of variants within the fat mass and obesity-associated (FTO) gene and polycystic ovary syndrome
Thomas Barber 1 , Amanda Bennett 1 , Christopher Groves 1 , Ulla Sovio 2 , Aimo Ruokonen 3 , Hannu Martikainen 3 , Anneli Pouta 3 , Anna-Liisa Hartikainen 3 , Paul Elliott 2 , Cecilia Lindgren 1 , Rachel Freathy 4 , Kirsten Koch 5 , Willem Ouwehand 5 , Fredrik Karpe 1 , Gerard Conway 6 , John Wass 1 , Marjo-Riitta Jarvelin 2 , Stephen Franks 2 & Mark McCarthy 1
1University of Oxford, Oxford, UK; 2Imperial College, London, UK; 3University of Oulu, Oulu, Finland; 4Peninsula Medical School, Exeter, UK; 5University of Cambridge, Cambridge, UK; 6University College Hospital, London, UK.
Background: Obesity plays an important role in the aetiology of polycystic ovary syndrome (PCOS). Variants in the fat-mass and obesity-associated (FTO) gene have recently been shown to influence adiposity and predispose to common obesity (Frayling et al., Science 2007 316 889–894).
Aim: Our aim was to establish whether FTO variants are also implicated in PCOS-susceptibility.
Methods: A genetic association study of FTO variant rs9939609 was conducted in 463 PCOS cases (geometric mean BMI 27.5 kg/m2) and 1336 female controls (geometric mean BMI 25.3 kg/m2) of UK British/Irish origin. We also sought evidence for associations between FTO variation and levels of circulating testosterone in 324 UK cases and 1000 women from the Northern Finland Birth Cohort of 1966 (NFBC1966). Measurements included FTO rs9939609 genotype frequencies by subject group, and androgen measures (testosterone, free androgen index) by genotype. The study was approved by the relevant local research ethics committees in the UK and Finland.
Results: There was a significant association between FTO genotype and PCOS status in the UK case–control analysis, which was attenuated by adjustment for BMI (Cochran-Armitage test, OR (per copy of the minor allele) 1.30 (95% CI 1.12–1.51), P=7.2×10−4 (unadjusted), P=2.9×10−3 (adjusted)). This association was most evident in obese PCOS cases (PCOS cases below median BMI versus UK controls, P=0.11; above median BMI versus controls, P=2.9×10−4). No relationship between FTO genotype and androgen levels was seen.
Conclusions: We provide the first evidence that variants that predispose to common obesity also result in altered susceptibility to PCOS, confirming the mechanistic link between these conditions. The attenuation of signal when adjusting for obesity indicates that the predominant effect of FTO variants on PCOS-susceptibility is mediated through adiposity.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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