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 beta-adrenergic receptor (ADRB3) genes have been linked to increased body mass index (BMI; in kg/m(2)), obesity, and more recently dietary nutrients and preferences. In addition, common variation in ADRB3 interacts with PPARG to modulate adult body weight. This study investigated whether variants in these genes were associated with measurable effects on child eating behavior. 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. 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). This is the first study to suggest that a genetic interaction involving ADRB3 and PPARG variants influences eating behavior in children.
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