Abstract
Variation in the peroxisome proliferator–activated receptor γ gene alters the risk for adiposity in adults, with evidence of interaction with diet.
We investigated the age-related association between the Pro12Ala variant (rs1801282)
and diet in obesity-related traits in children. The Pro12Ala variant was assayed in
2102 young children aged 1 to 6 years and in 794 periadolescent children aged 10 to
12 years of Greek origin. In both cohorts, no differences were found in obesity traits
between the Ala allele carriers and Pro/Pro homozygotes. Sex-stratified analysis showed
that, in periadolescent boys, Ala carriers exhibited lower measures of skinfolds (triceps:
16.9 ± 6.9 vs 19.4 ± 7.9 mm, P = .01; subscapular: 9.6 ± 4.5 vs 11.2 ± 5.4 mm, P = .02). On the other hand, young girls who were Ala carriers presented higher measures
of triceps skinfold thickness (10.5 ± 3.0 vs 9.9 ± 2.8 mm, P = .04). Nominal gene-diet interactions were revealed in periadolescents for saturated
fatty acid (SFA) intake and skinfolds (P for interaction = .05). In Pro/Pro homozygous young girls, SFA and total fat (TF)
intake was positively associated with higher body mass index (BMI) (P = .01), waist circumference (P = .02), and skinfold thickness (triceps-SFA: P = 10−5, triceps-TF: P = 10−9, subscapular-SFA: P = 10−6, subscapular-TF: P = 10−4). For Pro/Pro homozygotes, unsaturated fat intake was inversely associated with BMI
(P = .04) in young girls, and with BMI (P = .03), waist circumference (P = .03), and triceps (P = .02) in periadolescent boys. Our results suggest that adiposity in children is
influenced by the Pro12Ala polymorphism in a sex-specific and age-dependent manner.
We also demonstrate evidence of an age-dependent gene-diet (SFA, TF) interaction,
suggesting that the type of fat intake modifies the effect of the Pro12 allele on
obesity-related measures.
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Article info
Publication history
Published online: May 26, 2010
Accepted:
April 7,
2010
Received:
December 12,
2009
Identification
Copyright
© 2011 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
