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阿片受体 μ 型 1(OPRM1)基因 A118G(Asn40Asp)变异与吸烟起始、尼古丁依赖和戒烟关系的系统评价。

A systematic review of the A118G (Asn40Asp) variant of OPRM1 in relation to smoking initiation, nicotine dependence and smoking cessation.

机构信息

Behavioural Science Institute, Radboud University Nijmegen, PO Box 9104, 6500 HE Nijmegen, The Netherlands.

出版信息

Pharmacogenomics. 2012 Jun;13(8):917-33. doi: 10.2217/pgs.12.76.

DOI:10.2217/pgs.12.76
PMID:22676196
Abstract

Candidate gene studies on smoking behaviors mainly focused on dopaminergic and serotonergic genes, but genes within the µ-opioid system might also be involved. The A118G variant within the OPRM1 gene has been most often examined in relation to smoking, yielding inconsistent findings. It is largely unknown which of the alleles increases susceptibility for smoking behaviors. The aim of this review was to merge findings of OPRM1 gene studies in relation to smoking behaviors and to elaborate on the underlying biological mechanism of the A118G variant. It appeared that A118 was more likely to increase susceptibility to smoking behaviors than 118G, especially with regard to nicotine dependence, but less with smoking initiation and cessation. The proposed functioning of the OPRM1 gene is further explained.

摘要

候选基因研究主要集中在多巴胺能和 5-羟色胺能基因上,但阿片μ受体(OPRM1)系统内的基因也可能参与其中。阿片μ受体(OPRM1)基因 A118G 变体与吸烟行为的关系最常被研究,但结果并不一致。目前还不清楚哪种等位基因增加了吸烟行为的易感性。本综述的目的是综合阿片μ受体(OPRM1)基因与吸烟行为关系的研究结果,并阐述 A118G 变体的潜在生物学机制。结果表明,A118 比 118G 更有可能增加对吸烟行为的易感性,尤其是在尼古丁依赖方面,但在吸烟开始和戒烟方面则不然。进一步解释了阿片μ受体(OPRM1)基因的作用机制。

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