Article
Dietary Intake, FTO Genetic Variants, and Adiposity: A Combined Analysis of Over 16,000 Children and Adolescents
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- (1) Albert Einstein College of Medicine, grid.251993.5
- (2) Harvard University, grid.38142.3c
- (3) University of Copenhagen, grid.5254.6, KU
- (4) MRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke’s Hospital and University of Cambridge, Cambridge, U.K
- (5) Erasmus University Medical Center, grid.5645.2
- (6) University of Southampton, grid.5491.9
- (7) University of Leicester, grid.9918.9
- (8) Harokopio University, grid.15823.3d
- (9) Helmholtz Zentrum München, grid.4567.0
- (10) University of Split, grid.38603.3e
- (11) Wellcome Sanger Institute, grid.10306.34
- (12) University of Oulu, grid.10858.34
- (13) Leiden University, grid.5132.5
- (14) Leipzig University, grid.9647.c
- (15) Kuopion Liikuntalääketieteen Tutkimuslaitos, grid.419013.e
- (16) University of Eastern Finland, grid.9668.1
- (17) Capital Medical University, grid.24696.3f
- (18) Karolinska Institute, grid.4714.6
- (19) Yamaguchi University, grid.268397.1
- (20) Turku University Hospital, grid.410552.7
- (21) University of Turku, grid.1374.1
- (22) University of Bristol, grid.5337.2
- (23) University of Glasgow, grid.8756.c
- (24) Finnish Institute of Occupational Health, grid.6975.d
- (25) Augusta University, grid.410427.4
- (26) University Medical Center Groningen, grid.4494.d
- (27) Hokkaido Nursing College, Chuo-ku, Sapporo, Japan
- (28) Icahn School of Medicine at Mount Sinai, grid.59734.3c
- (29) Brigham and Women's Hospital, grid.62560.37
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The FTO gene harbors variation with the strongest effect on adiposity and obesity risk. Previous data support a role for FTO variation in influencing food intake. We conducted a combined analysis of 16,094 boys and girls aged 1-18 years from 14 studies to examine the following: 1) the association between the FTO rs9939609 variant (or a proxy) and total energy and macronutrient intake; and 2) the interaction between the FTO variant and dietary intake, and the effect on BMI. We found that the BMI-increasing allele (minor allele) of the FTO variant was associated with increased total energy intake (effect per allele = 14.3 kcal/day [95% CI 5.9, 22.7 kcal/day], P = 6.5 × 10(-4)), but not with protein, carbohydrate, or fat intake. We also found that protein intake modified the association between the FTO variant and BMI (interactive effect per allele = 0.08 SD [0.03, 0.12 SD], P for interaction = 7.2 × 10(-4)): the association between FTO genotype and BMI was much stronger in individuals with high protein intake (effect per allele = 0.10 SD [0.07, 0.13 SD], P = 8.2 × 10(-10)) than in those with low intake (effect per allele = 0.04 SD [0.01, 0.07 SD], P = 0.02). Our results suggest that the FTO variant that confers a predisposition to higher BMI is associated with higher total energy intake, and that lower dietary protein intake attenuates the association between FTO genotype and adiposity in children and adolescents.
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