Dopamine for "Wanting" and Opioids for "Liking": A Comparison of Obese Adults With and Without Binge Eating
Dopamine for "Wanting" and Opioids for "Liking": A Comparison of Obese Adults With and Without Binge Eating
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DOI：
10.1038/oby.2009.52
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发表时间：
2009-06-01
期刊：
影响因子：
6.9
通讯作者：
Kennedy, James L.
中科院分区：
文献类型：
--
作者：
Davis, Caroline A.;Levitan, Robert D.;Kennedy, James L.
肥胖研究遭受过度包容的范式，即所有参与者的BMI超过一定的截止值（e。例如，在一个实施例中，30)通常合并在一个组中，并与正常体重的人进行比较。很少有人试图通过显著的生物行为差异来确定有意义的亚组。为了解决这一局限性，我们研究了遗传和心理指标的享乐饮食在肥胖成人（n = 66）和（n = 70）暴食症（BED）。我们的分析集中在多巴胺（DA）和阿片类药物的遗传标记，因为它们与大脑奖励机制的功能相关联。我们针对与D2受体（DRD2）基因相关的三种功能多态性，以及μ阿片受体（OPRM 1）基因的功能A118G多态性。我们发现，与BED组相比，肥胖对照组有更多的Taq1A的"功能丧失" A1等位基因，而A118G的"功能获得" G等位基因在BED组中发生的频率更高。一个显著的基因-基因组合卡方（2）分析也表明，在那些具有增益-增益基因型（G（+）和A1）的参与者中，80%在BED组，而只有35%具有损失-损失基因型（G（-）和A1（+））在该组。最后，BED受试者在自我报告的享乐饮食测量中得分显著更高。我们的研究结果表明，BED是一种基于生物学的肥胖亚型，暴饮暴食的倾向可能受到对食物享乐特性的高反应性的影响，这种倾向在我们目前的环境中很容易被利用，因为我们非常容易看到和容易获得过量的甜食和脂肪食物。
Obesity research suffers from an overinclusion paradigm whereby all participants with a BMI beyond a certain cutoff value (e. g., 30) are typically combined in a single group and compared to those of normal weight. There has been little attempt to identify meaningful subgroups defined by their salient biobehavioral differences. In order to address this limitation, we examined genetic and psychological indicators of hedonic eating in obese adults with (n = 66) and without (n = 70) binge eating disorder (BED). Our analyses focused on dopamine (DA) and opioid genetic markers because of their conjoint association with the functioning of brain reward mechanisms. We targeted three functional polymorphisms related to the D2 receptor (DRD2) gene, as well as the functional A118G polymorphism of the mu-opioid receptor (OPRM1) gene. We found that significantly more obese controls had the "loss-of-function" A1 allele of Taq1A compared to their BED counterparts, whereas the "gain-of-function" G allele of A118G occurred with greater frequency in the BED group. A significant gene-gene combination chi(2) analysis also indicated that of those participants with the gain-gain genotype (G(+) and A1), 80% were in the BED group whereas only 35% with the loss-loss genotype (G(-) and A1(+)) were in this group. Finally, BED subjects had significantly higher scores on a self-report measure of hedonic eating. Our findings suggest that BED is a biologically based subtype of obesity and that the proneness to binge eating may be influenced by a hyper-reactivity to the hedonic properties of food-a predisposition that is easily exploited in our current environment with its highly visible and easily accessible surfeit of sweet and fatty foods.