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 γ (PPARG) and β-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.
- Body mass index
- Eating behavior
- Energy compensation
- Pparg gene variants