International Congress on Abnominal Obesity
Am J Clin Nutr 90: 1483-1488, 2009. First published October 14, 2009; doi:10.3945/ajcn.2009.28439
 American Journal of Clinical Nutrition, doi:10.3945/ajcn.2009.28439
Vol. 90, No. 6, 1483-1488, December 2009
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© 2009 American Society for Clinical Nutrition

ORIGINAL RESEARCH COMMUNICATION

The FTO gene rs9939609 obesity-risk allele and loss of control over eating1,2,3,4,5

Marian Tanofsky-Kraff, Joan C Han, Kavitha Anandalingam, Lauren B Shomaker, Kelli M Columbo, Laura E Wolkoff, Merel Kozlosky, Camden Elliott, Lisa M Ranzenhofer, Caroline A Roza, Susan Z Yanovski and Jack A Yanovski

1 From the Unit on Growth and Obesity, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, Bethesda, MD (MT-K, JCH, KA, LBS, KMC, LEW, CE, LMR, CAR, and JAY); Uniformed Services University of the Health Sciences, Bethesda, MD (MT-K, LBS, KMC, LEW, CE, and LMR); the Nutrition Department, Clinical Center, National Institutes of Health, Bethesda, MD (MK); and the Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services (SZY).

2 MT-K and JCH contributed equally to this work.

3 The opinions and assertions expressed herein are those of the authors and are not to be construed as reflecting the views of the Uniformed Services University of the Health Sciences or the US Department of Defense.

4 Supported by the Intramural Research Program, National Institute of Child Health, National Institutes of Health (grant Z01-HD-00641 to JAY), and supplemental funding from NCMHD (to JAY) and the Uniformed Services University of the Health Sciences (grant R072IC to MTK).

5 Address correspondence to JA Yanovski, Unit on Growth and Obesity, PDEGEN, NICHD, National Institutes of Health, 10 Center Drive, Hatfield Clinical Research Center, Room 1-3330, MSC 1103, Bethesda, MD 20892-1103. E-mail: jy15i{at}nih.gov.

Background: Children with rs9939609 FTO variant alleles (homozygous = AA and heterozygous = AT) are predisposed to greater adiposity than are those with 2 wild-type alleles (TT).

Objective: Because FTO is highly expressed in hypothalamic regions that are important for appetite, FTO genotype may affect energy balance by influencing eating behavior. Loss of control (LOC) eating, a behavior commonly reported by overweight youth, predicts excessive weight gain in children. However, the relation between FTO genotype and LOC eating has not been previously examined.

Design: Two-hundred eighty-nine youth aged 6–19 y were genotyped for rs9939609, underwent body-composition measurements, and were interviewed to determine the presence or absence of LOC eating. A subset (n = 190) participated in a lunch buffet test meal designed to model an LOC eating episode. Subjects with AA and AT genotypes were grouped together for comparison with wild-type TT subjects.

Results: Subjects with at least one A allele (67.7%) had significantly greater body mass indexes, body mass index z scores (P < 0.01), and fat mass (P < 0.05). Of the AA/AT subjects, 34.7% reported LOC compared with 18.2% of the TT subjects (P = 0.002). Although total energy intake at the test meal did not differ significantly by genotype (P = 0.61), AA/AT subjects consumed a greater percentage of energy from fat than did the TT subjects (P < 0.01).

Conclusions: Children and adolescents with 1 or 2 FTO rs9939609 obesity-risk alleles report more frequent LOC eating episodes and select foods higher in fat at a buffet meal. Both LOC eating and more frequent selection of energy-dense, palatable foods may be mechanisms through which variant FTO alleles lead to excess body weight.