Yeum Dabin, Renier Timothy J, Masterson Travis D, Carlson Delaina D, Ballarino Grace A, Lansigan Reina K, Loos Ruth J F, Emond Jennifer A, Gilbert-Diamond Diane
Department of Epidemiology, Geisel School of Medicine at Dartmouth College, Lebanon, New Hampshire, USA.
Department of Nutritional Sciences, College of Health and Human Development, The Pennsylvania State University, University Park, Pennsylvania, USA.
Pediatr Obes. 2025 Apr;20(4):e13168. doi: 10.1111/ijpo.13168. Epub 2024 Aug 28.
The objective of this study is to evaluate obesity-related genetic factors in relation to excess consumption and assess if food cues modify associations.
Children (9-12 years) completed a randomized crossover experiment. During two visits, children ate a preload and then snacks ad libitum while watching television, embedded with food or non-food advertisements to assess eating in the absence of hunger (EAH). Primary exposures were obesity-associated genotypes, FTO rs9939609 and MC4R rs571312, and a paediatric-specific polygenic risk score (PRS). Outcomes included consumption of all snacks (total EAH) and gummy candy only (gummy candy EAH). Linear mixed-effects models tested whether genetic exposures related to EAH outcomes. We tested for effect modification by food cues using multiplicative interaction terms.
Among 177 children, each FTO risk allele was associated with a 30% increase in gummy candy EAH (p = 0.025) in adjusted models. Food cue exposure exacerbated associations between the FTO variant with gummy candy EAH (p = 0.046). No statistically significant associations were found between MC4R and EAH.
The results suggest children with the FTO rs9939609 risk allele may be predisposed to excess consumption of candy and that this association may be exacerbated by food cues.
本研究的目的是评估与过量摄入相关的肥胖相关遗传因素,并评估食物线索是否会改变这种关联。
儿童(9至12岁)完成了一项随机交叉实验。在两次访视期间,儿童先吃一顿预负荷餐,然后在看电视时随意吃零食,电视中嵌入了食物或非食物广告,以评估在无饥饿状态下的进食情况(EAH)。主要暴露因素为肥胖相关基因型,即FTO rs9939609和MC4R rs571312,以及儿童特异性多基因风险评分(PRS)。结局指标包括所有零食的摄入量(总EAH)和仅软糖的摄入量(软糖EAH)。线性混合效应模型测试了遗传暴露与EAH结局之间的关系。我们使用乘法交互项测试了食物线索的效应修饰作用。
在177名儿童中,在调整模型中,每个FTO风险等位基因与软糖EAH增加30%相关(p = 0.025)。食物线索暴露加剧了FTO变异体与软糖EAH之间的关联(p = 0.046)。未发现MC4R与EAH之间存在统计学上的显著关联。
结果表明,携带FTO rs9939609风险等位基因的儿童可能易患糖果过量摄入,且这种关联可能会因食物线索而加剧。