美國科羅拉多大學一項新的研究表明,，你的遺傳決定你能夠比別人喝的更多,，而且不會增加酒精中毒或酒精依賴的風險,。這項研究指出了具體的遺傳通路以及酒精消耗水平相關的基因,，該基因與人類和老鼠中的酒精依賴無關,。
研究小組使用老鼠對影響酒精消耗行為的遺傳通路進行識別。他們發(fā)現(xiàn)老鼠的飲酒行為與大腦中的快樂和獎賞通路（the pleasure and reward pathways）有關,，也與一些控制對食物的滿足和欲望的遺傳系統(tǒng)有關,。接下來研究人員對老鼠和人類中酒精相關通路中的基因進行比對，試著識別出與酒精消耗有關的普遍遺傳因子,。
結(jié)果是很新奇的,，所識別的基因與試驗人群的飲酒行為有關，但與酒精依賴并不是同一個基因,。
Tabakoff介紹說,，我們知道，在那些遺傳學上更傾向于依賴的人群中,，高水平的酒精消耗會增加酒精依賴的風險,。事實上,，在這項研究中，我們發(fā)現(xiàn)人類中高水平的酒精消耗與酒精依賴是絕對正相關的,。然而,，由于似乎是不同的基因影響酒精消耗的水平，有的會抵抗酒精依賴的趨勢,，所以在人類中存在很大的變動,。
那些含有趨向于消耗適量酒精的遺傳學個體可能仍然有一個遺傳學趨勢會對飲酒行為失去控制，并可能發(fā)展成酒精依賴,。相反的,，能夠飲用大量酒精的遺傳學個體可能并沒有趨向于酒精依賴的基因。
作者強調(diào)說,，在本文中研究的表型并不依賴于酒精攝入，是基因影響了這些表型,。（生物谷Bioon.com）
酒精與健康研究：
PNAS：饑餓激素可能影響酒精依賴
JCBFM：飲酒6分鐘后酒精即“上頭”
PNAS：酒精易感性的遺傳聯(lián)系
Am.J.Med：中年人適量飲酒可預防心血管疾病
Alcohol：酒精具有免疫調(diào)節(jié)作用
生物谷推薦原始出處：
BMC Biology 2009, 7:70doi:10.1186/1741-7007-7-70
Genetical genomic determinants of alcohol consumption in rats and humans
Boris Tabakoff , Laura Saba , Morton Printz , Pam Flodman , Colin Hodgkinson , David Goldman , George Koob , Heather N Richardson , Katerina Kechris , Richard L Bell , Norbert Hubner , Matthias Heinig , Michal Pravenec , Jonathan Mangion , Lucie Legault , Maurice Dongier , Katherine M Conigrave , John B Whitfield , John Saunders , Bridget Grant , Paula L Hoffman and WHO/ISBRA Study on State and Trait Markers of Alcoholism
Background
We have used a genetical genomic approach, in conjunction with phenotypic analysis of alcohol consumption, to identify candidate genes that predispose to varying levels of alcohol intake by HXB/BXH recombinant inbred rat strains. In addition, in two populations of humans, we assessed genetic polymorphisms associated with alcohol consumption using a custom genotyping array for 1,350 single nucleotide polymorphisms (SNPs). Our goal was to ascertain whether our approach, which relies on statistical and informatics techniques, and non-human animal models of alcohol drinking behavior, could inform interpretation of genetic association studies with human populations.
Results
In the HXB/BXH recombinant inbred (RI) rats, correlation analysis of brain gene expression levels with alcohol consumption in a two-bottle choice paradigm, and filtering based on behavioral and gene expression quantitative trait locus (QTL) analyses, generated a list of candidate genes. A literature-based, functional analysis of the interactions of the products of these candidate genes defined pathways linked to presynaptic GABA release, activation of dopamine neurons, and postsynaptic GABA receptor trafficking, in brain regions including the hypothalamus, ventral tegmentum and amygdala. The analysis also implicated energy metabolism and caloric intake control as potential influences on alcohol consumption by the recombinant inbred rats. In the human populations, polymorphisms in genes associated with GABA synthesis and GABA receptors, as well as genes related to dopaminergic transmission, were associated with alcohol consumption.
Conclusions
Our results emphasize the importance of the signaling pathways identified using the non-human animal models, rather than single gene products, in identifying factors responsible for complex traits such as alcohol consumption. The results suggest cross-species similarities in pathways that influence predisposition to consume alcohol by rats and humans. The importance of a well-defined phenotype is also illustrated. Our results also suggest that different genetic factors predispose alcohol dependence versus the phenotype of alcohol consumption.
