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The fat mass–and obesity-associated locus and dietary intake in children^1,2,3

¹ MRC CAiTE Centre, Department of Social Medicine (NJT and GDS) and the Department of Community Based Medicine (PME), Bristol University, Bristol, United Kingdom; Genetics of Complex Traits (TMF and ATH) and Diabetes Genetics (TMF and ATH), Institute of Biomedical and Clinical Science, Peninsula Medical School, Exeter, United Kingdom; the School of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, United Kingdom (IR); the Oxford Centre for Diabetes, Endocrinology and Metabolism (MIM) and the Wellcome Trust Centre for Human Genetics (NJT and MIM), University of Oxford, Oxford, United Kingdom

Background: A region of chromosome 16 containing the fat mass–and obesity-associated gene (FTO) is reproducibly associated with fat mass and body mass index (BMI), risk of obesity, and adiposity.

Objectives: We aimed to assess the possibility that appetite plays a role in the association between FTO and BMI.

Design: Detailed dietary report information from the Avon Longitudinal Study of Parents and Children allowed the exploration of relations between FTO variation and dietary intake. Analyses were performed to investigate possible associations between variation at the FTO locus and the intake of a range of micronutrients and macronutrients, with adjustment for the bias often found within dietary report data when factors related to BMI are assessed. To test the hypothesis that FTO may be influencing appetite directly, rather than indirectly via BMI and altered intake requirements, we also assessed associations between FTO and dietary intake independent of BMI.

Results: Relations between a single-nucleotide polymorphism characterizing the FTO signal (rs9939609) and dietary variables were found and can be summarized by the effect of each additional allele (per-allele effects) on total energy and total fat (P < 0.001 for both). These associations were attenuated, but they persisted specifically for fat and energy consumption after adjustment for BMI [total daily fat consumption: 1.5 g/d (P = 0.02 for the per-allele difference); total daily energy consumption: 25 kJ/d (P = 0.03 for the per-allele difference)].

Conclusion: These associations suggest that persons carrying minor variants at rs9939609 were consuming more fat and total energy than were those not carrying such variants. They also suggest that this difference was not simply dependent on having higher average BMIs among the former group.