Institute of Nutrition and Functional Foods (INAF).
School of Nutrition.
Am J Clin Nutr. 2018 Sep 1;108(3):445-452. doi: 10.1093/ajcn/nqy130.
Genome-wide association studies (GWASs) have identified several genes associated with obesity. The mechanisms through which these genes affect body weight are not fully characterized. Recent studies suggest that eating behavior (EB) traits could be involved, but only a few EB traits were investigated.
This study aimed to investigate whether genetic susceptibility to obesity is mediated by EB traits (cognitive restraint, disinhibition, hunger) and their subscales. We hypothesized that EB traits, and their subscales, partly mediate this association.
Adult individuals (n = 768) who participated in the Quebec Family Study were included in this cross-sectional study. A genetic risk score (GRS) of obesity was calculated based on the 97 genetic variants recently identified in a GWAS meta-analysis of body mass index (BMI). EB traits and their subscales were assessed with the use of the Three-Factor Eating Questionnaire. Regression analyses with age and sex as covariates were used to investigate the associations between GRS, EB traits, BMI, and WC and whether the association between GRS and obesity is mediated by EB traits, which represents the indirect effect of GRS on obesity.
The GRS of obesity was positively associated with BMI (β = 0.19 ± 0.04, P < 0.0001) and WC (β = 0.46 ± 0.10, P < 0.0001). Regression analyses also revealed that the association between GRS of obesity and BMI was partly mediated by disinhibition and susceptibility to hunger (βindirect = 0.09 ± 0.03, P = 0.0007, and βindirect = 0.04 ± 0.02, P = 0.02, respectively). Habitual and situational susceptibility to disinhibition (βindirect = 0.08 ± 0.03, P = 0.002 and βindirect = 0.05 ± 0.02, P = 0.003, respectively) as well as internal and external locus of hunger (βindirect = 0.03 ± 0.02, P = 0.03 for both) were also found to mediate the association between GRS of obesity and BMI. The same trends were observed with WC.
The results of this study indicate that the genetic susceptibility to obesity is partly mediated through undesirable EB traits, which suggests that they could be targeted in obesity treatment and prevention. This trial was registered at clinicaltrials.gov as NCT03355729.
全基因组关联研究（GWAS）已经鉴定出了一些与肥胖相关的基因。这些基因影响体重的机制尚未完全阐明。最近的研究表明，饮食行为（EB）特征可能与之相关，但只研究了少数几个 EB 特征。
本研究旨在探讨肥胖的遗传易感性是否通过 EB 特征（认知约束、抑制失控、饥饿）及其亚量表来介导。我们假设 EB 特征及其亚量表部分介导了这种关联。
本横断面研究纳入了参加魁北克家庭研究的 768 名成年个体。基于最近在 BMI 荟萃分析的 GWAS 中鉴定的 97 个遗传变异，计算了肥胖的遗传风险评分（GRS）。使用 Three-Factor Eating Questionnaire 评估 EB 特征及其亚量表。采用包含年龄和性别作为协变量的回归分析，探讨了 GRS、EB 特征、BMI 和 WC 之间的关联，以及 GRS 与肥胖之间的关联是否通过 EB 特征来介导，这代表了 GRS 对肥胖的间接影响。
肥胖的 GRS 与 BMI（β=0.19±0.04，P<0.0001）和 WC（β=0.46±0.10，P<0.0001）呈正相关。回归分析还表明，肥胖的 GRS 与 BMI 之间的关联部分通过抑制失控和饥饿易感性来介导（β间接=0.09±0.03，P=0.0007，和 β间接=0.04±0.02，P=0.02）。习惯性和情境性抑制失控易感性（β间接=0.08±0.03，P=0.002 和 β间接=0.05±0.02，P=0.003）以及内部和外部饥饿源（β间接=0.03±0.02，P=0.03）也被发现介导了肥胖的 GRS 与 BMI 之间的关联。在 WC 方面也观察到了相同的趋势。
本研究结果表明，肥胖的遗传易感性部分通过不良的 EB 特征来介导，这表明它们可能成为肥胖治疗和预防的目标。该试验在 clinicaltrials.gov 上注册为 NCT03355729。
