Gene-by-Activity Interactions on Obesity Traits of 6-Year-Old New Zealand European Children: A Children of SCOPE Study

in Pediatric Exercise Science
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Purpose: The decline of physical activity in children is considered an important determinant to explain the rising rates of obesity. However, this risk may be augmented in children who are genetically susceptible to increased weight gain. We hypothesized that a sedentary lifestyle and moderate activity will interact with genetic loci, resulting in differential effects in relation to obesity risk. Methods: We recruited 643 European children born to participants in the New Zealand-based Screening for Pregnancy Endpoints (SCOPE) study. Seventy gene variants were evaluated by the Sequenom assay. Interaction analyses were performed between the genetic variants and the activity type derived from actigraphy, in relation to percentage body fat. Results: We found a statistically significant association between increased proportions of sedentary activity with increased percentage body fat scores (P = .012). The OLFM4-9568856 (P = .01) and GNPDA2-rs10938397 (P = .044) gene variants showed genotype differences with proportions of sedentary activity. Similarly, the OLFM4-9568856 (P = .021), CLOCK-rs4864548 (P = .029), and LEPR-1045895 (P = .047) showed genotype differences with proportions of moderate activity. We found evidence for unadjusted gene-by-activity interactions of SPACA3/SPRASA-rs16967845, PFKP-rs6602024, and SH2B1-rs7498665 on percentage body fat scores. Conclusions: These findings indicate a differential effect of physical activity in relation to obesity risk, suggesting that children genetically predisposed to increased weight gain may benefit from higher levels of moderate activity.

Krishnan, Shelling, McCowan, and Thompson are with the Dept. of Obstetrics and Gynaecology, University of Auckland, Auckland, New Zealand. Wall is with the Dept. of Nutrition and Dietetics, University of Auckland, Auckland, New Zealand. Mitchell and Thompson are with the Dept. of Paediatrics: Child & Youth Health, University of Auckland, Auckland, New Zealand. Murphy is with the Dept. of Medicine, University of Auckland, Auckland, New Zealand; and Maurice Wilkins Centre for Biodiscovery, University of Auckland, Auckland, New Zealand. *New Zealand: W. Cutfield is with the Liggins Institute, University of Auckland, Auckland; Y. Huang is with the School of Population Health, University of Auckland, Auckland; A. Stewart is with the School of Population Health, University of Auckland, Auckland; R. Taylor is with the Department of Obstetrics and Gynaecology, University of Auckland, Auckland). United Kingdom: K.M. Godfrey is with the MRC Lifecourse Epidemiology Unit and NIHR Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust; L. Poston is with the Division of Women’s Health, King’s College London, St Thomas’ Hospital, London; P. Taylor is with the Division of Women’s Health, King’s College London, St Thomas’ Hospital, London.

Address author correspondence to John M.D. Thompson at j.thompson@auckland.ac.nz.

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