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在一个大型社区样本中,儿茶酚-O-甲基转移酶(COMT)的甲硫氨酸等位基因对异常饮食的风险和严重程度有不同的预测作用。

COMT met allele differentially predicts risk versus severity of aberrant eating in a large community sample.

作者信息

Donofry Shannon D, Roecklein Kathryn A, Wildes Jennifer E, Miller Megan A, Flory Janine D, Manuck Stephen B

机构信息

Department of Psychology, University of Pittsburgh, Pittsburgh, PA, USA.

Department of Psychology, University of Pittsburgh, Pittsburgh, PA, USA; Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, PA, USA.

出版信息

Psychiatry Res. 2014 Dec 15;220(1-2):513-8. doi: 10.1016/j.psychres.2014.08.037. Epub 2014 Aug 27.

Abstract

Prefrontal dopamine (DA) transmission participates in the reinforcement of reward-driven behaviors like eating. Because catechol-O-methyltransferase (COMT) degrades DA and is expressed in the prefrontal cortex, variation in the COMT gene may modulate eating behavior. Previous studies have shown that the met allele of the COMT val158met single nucleotide polymorphism (SNP) is associated with Bulimia Nervosa (BN). The specific aim of this study was to test whether the met allele increased risk for, and severity of, eating disorder symptomatology in community volunteers. Caucasian adults (N=1003; 51.2% female) from the University of Pittsburgh Adult Health and Behavior Project (AHAB) were genotyped and completed the Eating Disorders Inventory (EDI). Logistic and Poisson regression analyses assessed genotype-dependent presence and severity of eating disorder symptomatology. The met allele was significantly associated with the presence of symptoms on the Bulimia subscale and the severity of Body Dissatisfaction scores. All EDI subscales significantly predicted BMI. To our knowledge, these are the first data indicating that the COMT met allele increases risk for some symptoms of disordered eating, while increasing severity of others, in a community sample. These novel findings may have important implications for understanding the etiology of heterogeneous disordered eating phenotypes.

摘要

前额叶多巴胺(DA)传递参与强化进食等奖励驱动行为。由于儿茶酚-O-甲基转移酶(COMT)可降解DA且在前额叶皮质中表达,COMT基因的变异可能会调节进食行为。先前的研究表明,COMT基因val158met单核苷酸多态性(SNP)的met等位基因与神经性贪食症(BN)有关。本研究的具体目的是测试met等位基因是否会增加社区志愿者出现饮食失调症状的风险及严重程度。对来自匹兹堡大学成人健康与行为项目(AHAB)的白种成年人(N = 1003;51.2%为女性)进行基因分型,并让他们完成饮食失调量表(EDI)。逻辑回归和泊松回归分析评估了饮食失调症状的基因型依赖性存在情况和严重程度。met等位基因与神经性贪食症分量表上症状的存在以及身体不满得分的严重程度显著相关。所有EDI分量表都能显著预测体重指数(BMI)。据我们所知,这些是首批数据,表明在社区样本中,COMT基因的met等位基因会增加某些饮食失调症状的风险,同时增加其他症状的严重程度。这些新发现可能对理解异质性饮食失调表型的病因具有重要意义。

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