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American Journal of Clinical Nutrition, Vol. 86, No. 1, 167-173, July 2007
© 2007 American Society for Nutrition


ORIGINAL RESEARCH COMMUNICATION

Variants of the peroxisome proliferator-activated receptor {gamma}- and ß-adrenergic receptor genes are associated with measures of compensatory eating behaviors in young children1,2,3

Joanne E Cecil, Colin NA Palmer, Bettina Fischer, Peter Watt, Deborah J Wallis, Inez Murrie and Marion M Hetherington

1 From the Bute Medical School, University of St Andrews, St Andrews, Scotland (JEC); the Biomedical Research Centre, Ninewells Hospital and Medical School, University of Dundee, Dundee, Scotland (CNAP, BF, and IM); the Chelsea School, University of Brighton, Brighton, United Kingdom (PW); the Department of Human Sciences, Loughborough University, Leicestershire, United Kingdom (DJW); and the Department of Psychology, Glasgow Caledonian University, Glasgow, Scotland (MMH)

Background: Young children can regulate energy precisely in the short term, showing the potential for an innate compensation mechanism of eating behavior. However, data suggest that precise compensation is attenuated as a function of increasing adiposity, parental feeding style, and age. Common variation in candidate obesity genes may account for some of the individual variation observed in short-term energy compensation. Polymorphisms in the peroxisome proliferator-activated receptor {gamma} (PPARG) and ß-adrenergic receptor (ADRB3) genes have been linked to increased body mass index (BMI; in kg/m2), obesity, and more recently dietary nutrients and preferences. In addition, common variation in ADRB3 interacts with PPARG to modulate adult body weight.

Objective: This study investigated whether variants in these genes were associated with measurable effects on child eating behavior.

Design: Children (n = 84) aged 4–10 y were prospectively selected for variants of the PPARG locus (Pro12Ala, C1431T). Heights and weights were measured. Energy intake from a test meal was measured 90 min after ingestion of a no-energy (NE), low-energy (LE), or high-energy (HE) preload, and the compensation index (COMPX) was calculated.

Results: BMI differed significantly by gene model, whereby Pro12Ala was associated with a lower BMI. Poor COMPX was associated with the PPARG T1431 allele (P = 0.009). There was a significant interaction between COMPX and the ADRB3 Trp64Arg variant in modulating compensation (P = 0.003), whereas the Arg64 allele was associated with good compensation (P = 0.001).

Conclusions: This is the first study to suggest that a genetic interaction involving ADRB3 and PPARG variants influences eating behavior in children.

Key Words: Children • eating behavior • energy compensation • PPARG gene variants • BMI • body mass index







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