2012年11月23日 讯 /生物谷BIOON/ --为什么有些人比其他人更幸福？一项新研究证实基因FTO是一个显著与肥胖有关的基因，也能使得一个人发展患抑郁症的概率减少8％，相关研究由加拿大麦克马斯特大学研究人员完成，研究结果最近发表在Molecular Psychiatry杂志上。
临床流行病学和生物统计学副教授David Meyre指出：FTO不仅是一种与肥胖有关的基因，也是一个与幸福快乐有关的基因。
报告指出，早前一项针对双胞胎和兄弟姐妹的试验结果显示抑郁症的遗传因素占40%，但后续试图找出基因与抑郁症之间的关联，令人惊讶却是失败的，并没有发现任何证据能显示两者之间有关联。
另一方面，许多人认为抑郁症患者往往肥胖，因为它们不会积极的生活。2010年的一项研究证实肥胖和抑郁症有联系。
Meyre继续说，我们的假设是忧郁和肥胖都与大脑活动有关。我们推测肥胖基因可能与抑郁症有关。专家们分析了参与EpiDREAM研究中，21个不同国家的17,200 DNA样本的遗传信息和精神状态。
科学家们发现，更容易发生FTO基因遗传改变患者，发展患抑郁症的概率减少了8％。专家们通过3个大型的全球性研究参与者的基因状态验证了他们的发现。
Meyre指出：该研究排除了FTO肥胖基因对身体质量系数的影响，是首次有证据表明了该基因和抑制严重抑郁有关联。Samaan说，这是一个重要的发现，抑郁症是一种常见的疾病，每五个加拿大人就有一位受抑郁症影响。（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.
