2012年11月23日 訊 /生物谷BIOON/ --為什么有些人比其他人更幸福,？一項(xiàng)新研究證實(shí)基因FTO是一個(gè)顯著與肥胖有關(guān)的基因,，也能使得一個(gè)人發(fā)展患抑郁癥的概率減少8％,，相關(guān)研究由加拿大麥克馬斯特大學(xué)研究人員完成,，研究結(jié)果最近發(fā)表在Molecular Psychiatry雜志上,。
臨床流行病學(xué)和生物統(tǒng)計(jì)學(xué)副教授David Meyre指出：FTO不僅是一種與肥胖有關(guān)的基因,，也是一個(gè)與幸?？鞓酚嘘P(guān)的基因,。
報(bào)告指出，早前一項(xiàng)針對(duì)雙胞胎和兄弟姐妹的試驗(yàn)結(jié)果顯示抑郁癥的遺傳因素占40%,，但后續(xù)試圖找出基因與抑郁癥之間的關(guān)聯(lián),，令人驚訝卻是失敗的，并沒有發(fā)現(xiàn)任何證據(jù)能顯示兩者之間有關(guān)聯(lián),。
另一方面,，許多人認(rèn)為抑郁癥患者往往肥胖，因?yàn)樗鼈儾粫?huì)積極的生活,。2010年的一項(xiàng)研究證實(shí)肥胖和抑郁癥有聯(lián)系,。
Meyre繼續(xù)說(shuō)，我們的假設(shè)是憂郁和肥胖都與大腦活動(dòng)有關(guān),。我們推測(cè)肥胖基因可能與抑郁癥有關(guān),。專家們分析了參與EpiDREAM研究中，21個(gè)不同國(guó)家的17,200 DNA樣本的遺傳信息和精神狀態(tài),。
科學(xué)家們發(fā)現(xiàn),，更容易發(fā)生FTO基因遺傳改變患者，發(fā)展患抑郁癥的概率減少了8％,。專家們通過(guò)3個(gè)大型的全球性研究參與者的基因狀態(tài)驗(yàn)證了他們的發(fā)現(xiàn),。
Meyre指出：該研究排除了FTO肥胖基因?qū)ι眢w質(zhì)量系數(shù)的影響,，是首次有證據(jù)表明了該基因和抑制嚴(yán)重抑郁有關(guān)聯(lián)。Samaan說(shuō),，這是一個(gè)重要的發(fā)現(xiàn),，抑郁癥是一種常見的疾病，每五個(gè)加拿大人就有一位受抑郁癥影響,。（生物谷：Bioon.com）
doi:10.1038/mp.2012.160
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The protective effect of the obesity-associated rs9939609 A variant in fat mass- and obesity-associated gene on depression
Z Samaan, S Anand, X Zhang, D Desai, M Rivera, G Pare, L Thabane, C Xie, H Gerstein, J C Engert, I Craig, S Cohen-Woods, V Mohan, R Diaz, X Wang, L Liu, T Corre, M Preisig, Z Kutalik, S Bergmann, P Vollenweider, G Waeber, S Yusuf and D Meyre
Candidate gene and genome-wide association studies have not identified common variants, which are reliably associated with depression. The recent identification of obesity predisposing genes that are highly expressed in the brain raises the possibility of their genetic contribution to depression. As variation in the intron 1 of the fat mass- and obesity-associated (FTO) gene contributes to polygenic obesity, we assessed the possibility that FTO gene may contribute to depression in a cross-sectional multi-ethnic sample of 6561 depression cases and 21??932 controls selected from the EpiDREAM, INTERHEART, DeCC (depression case–control study) and Cohorte Lausannoise (CoLaus) studies. Major depression was defined according to DSM IV diagnostic criteria. Association analyses were performed under the additive genetic model. A meta-analysis of the four studies showed a significant inverse association between the obesity risk FTO rs9939609 A variant and depression (odds ratio=0.92 (0.89, 0.97), P=3 × 10??4) adjusted for age, sex, ethnicity/population structure and body-mass index (BMI) with no significant between-study heterogeneity (I2=0%, P=0.63). The FTO rs9939609 A variant was also associated with increased BMI in the four studies (β 0.30 (0.08, 0.51), P=0.0064) adjusted for age, sex and ethnicity/population structure. In conclusion, we provide the first evidence that the FTO rs9939609 A variant may be associated with a lower risk of depression independently of its effect on BMI. This study highlights the potential importance of obesity predisposing genes on depression.
