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ORIGINAL RESEARCH COMMUNICATION |
1 From the MRC Epidemiology Unit, Institute of Metabolic Science, Cambridge, United Kingdom (KSV, SL, JHZ, JL, UE, NJW, and RJFL); the CNC, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom (SAB); and the Department of Public Health and Primary Care, Institute of Public Health, University of Cambridge, United Kingdom (K-TK).
2 The EPIC-Norfolk study is supported by program grants from the Medical Research Council UK and Cancer Research UK and with additional support from the European Union, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency, and the Wellcome Trust. 3 Address correspondence to RJF Loos, MRC Epidemiology Unit, Institute of Metabolic Science, Box 285, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, United Kingdom. E-mail: ruth.loos{at}mrc-epid.cam.ac.uk.
Background: Intronic variation in the FTO (fat mass and obesity-associated) gene has been unequivocally associated with increased body mass index (BMI; in kg/m2) and the risk of obesity in populations of different ethnicity.
Objective: We examined whether this robust genetic predisposition to obesity can be attenuated by being more physically active.
Design: The FTO variant rs1121980 was genotyped in 20,374 participants (39–79 y of age) from the European Prospective Investigation into Cancer and Nutrition–Norfolk Study, an ethnically homogeneous population-based cohort. Physical activity (PA) was assessed with a validated self-reported questionnaire. The interaction between rs1121980 and PA on BMI and waist circumference (WC) was examined by including the interaction term in mixed-effect models.
Results: We confirmed that the risk (T) allele of rs1121980 was significantly associated with BMI (0.31-unit increase per allele; P < 0.001) and WC (0.77-cm increase per allele; P < 0.001). The PA level attenuated the effect of rs1121980 on BMI and WC; ie, whereas in active individuals the risk allele increased BMI by 0.25 per allele, the increase in BMI was significantly (P for interaction = 0.004) more pronounced (76%) in inactive individuals (0.44 per risk allele). We observed similar effects for WC (P for interaction = 0.02): the risk allele increased WC by 1.04 cm per allele in inactive individuals but by only 0.64 cm in active individuals.
Conclusions: Our results showed that PA attenuates the effect of the FTO rs1121980 genotype on BMI and WC. This observation has important public health implications because we showed that a genetic susceptibility to obesity induced by FTO variation can be overcome, at least in part, by adopting a physically active lifestyle.
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  M. Tanofsky-Kraff, J. C Han, K. Anandalingam, L. B Shomaker, K. M Columbo, L. E Wolkoff, M. Kozlosky, C. Elliott, L. M Ranzenhofer, C. A Roza, et al. The FTO gene rs9939609 obesity-risk allele and loss of control over eating Am. J. Clinical Nutrition, December 1, 2009; 90(6): 1483 - 1488. [Abstract] [Full Text] [PDF]
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E. Sonestedt, C. Roos, B. Gullberg, U. Ericson, E. Wirfalt, and M. Orho-Melander Fat and carbohydrate intake modify the association between genetic variation in the FTO genotype and obesity Am. J. Clinical Nutrition, November 1, 2009; 90(5): 1418 - 1425. [Abstract] [Full Text] [PDF]
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