Yeum Dabin, Renier Timothy J, Carlson Delaina D, Ballarino Grace A, Lansigan Reina K, Meyer Meghan L, Loos Ruth J F, Emond Jennifer A, Masterson Travis D, Gilbert-Diamond Diane
Department of Epidemiology, Geisel School of Medicine at Dartmouth College, Lebanon, NH, United States.
Department of Pediatrics, Geisel School of Medicine at Dartmouth College, Lebanon, NH, United States.
Front Nutr. 2024 Sep 25;11:1387514. doi: 10.3389/fnut.2024.1387514. eCollection 2024.
To test associations of candidate obesity-related single nucleotide polymorphisms (SNPs) and obesity polygenic risk scores (PRS) with neural reward reactivity to food cues.
After consuming a pre-load meal, 9-12-year-old children completed a functional magnetic resonance imaging (fMRI) paradigm with exposure to food and non-food commercials. Genetic exposures included rs9939609, rs571312, and a pediatric-specific obesity PRS. A targeted region-of-interest (ROI) analysis for 7 bilateral reward regions and a whole-brain analysis were conducted. Independent associations between each genetic factor and reward responsivity to food cues in each ROI were evaluated using linear models.
Analyses included 151 children ( = 10.9 years). Each rs9939609 obesity risk allele was related to a higher food-cue-related response in the right lateral hypothalamus after controlling for covariates including the current BMI -score < 0.01), however, the association did not remain significant after applying the multiple testing correction. rs571312 and the PRS were not related to heightened food-cue-related reward responsivity in any examined regions. The whole-brain analysis did not identify additional regions of food-cue-related response related to the examined genetic factors.
Children genetically at risk for obesity, as indicated by the genotype, may be predisposed to higher food-cue-related reward responsivity in the lateral hypothalamus in the sated state, which, in turn, could contribute to overconsumption.
https://clinicaltrials.gov/study/NCT03766191, identifier NCT03766191.
检验与肥胖相关的候选单核苷酸多态性（SNP）和肥胖多基因风险评分（PRS）与对食物线索的神经奖赏反应性之间的关联。
在食用一顿预负荷餐后，9至12岁的儿童完成了一项功能性磁共振成像（fMRI）范式，期间暴露于食物和非食物广告。基因暴露包括rs9939609、rs571312以及一个儿科特异性肥胖PRS。对7个双侧奖赏区域进行了靶向感兴趣区域（ROI）分析和全脑分析。使用线性模型评估每个遗传因素与每个ROI中对食物线索的奖赏反应性之间的独立关联。
分析纳入了151名儿童（平均年龄 = 10.9岁）。在控制包括当前BMI评分在内的协变量后，rs9939609的每个肥胖风险等位基因与右侧下丘脑更高的食物线索相关反应有关（P < 0.01），然而，在应用多重检验校正后，该关联不再显著。rs571312和PRS与任何检查区域中增强的食物线索相关奖赏反应性均无关。全脑分析未发现与所检查的遗传因素相关的其他食物线索相关反应区域。
如rs9939609基因型所示，具有肥胖遗传风险的儿童在饱腹状态下可能易在下丘脑外侧对食物线索产生更高的奖赏反应性，这反过来可能导致过度消费。
https://clinicaltrials.gov/study/NCT03766191，标识符NCT03766191。
