此前有研究指出，蛋白质“Sirtuin”（去乙酰化酶）有助于很多生物延长寿命，然而发表于9月22日出版的《自然》杂志的最新研究显示，Sirtuin实际上与动物长寿无关。
科学研究曾认为，Sirtuin同酵母、小线虫以及果蝇（科学家们一般使用这些生物作为模型研究人类衰老）的衰老和长寿有关。也有研究证明，当生物体的基因过度制造Sirtuin时，其寿命会显著增加，线虫的寿命可增加50%。近来也有研究发现，节食能激活生物体制造出更多Sirtuin，而节食能延长包括哺乳动物在内的很多生物体的寿命早已获科学界承认。
Sirtuin引起了科学界的广泛关注，有人甚至将制造Sirtuin的基因称为“长寿基因”。很多护肤品公司宣称，抗衰老产品内添加的白藜芦醇能激活Sirtuin。而由英国伦敦大学学院健康老龄化研究所副所长戴维斯•杰姆斯领导的科研团队公布的最新研究认为，以前实验中出现的动物寿命的增加实际上与Sirtuin无关。
研究人员首先检查了以前两个不同实验所研究的两种不同的线虫，这些线虫的基因经过修改以使Sirtuin基因被过度激活。结果显示，与没有进行遗传修改的对照组线虫相比，遗传修改后的线虫寿命更长。随后，研究人员通过一些手段使两组线虫之间的唯一区别是Sirtuin的浓度不同，结果长寿现象消失了。这表明，造成此前出现长寿现象的原因是其他遗传因素。科学家们在其中一种没经过遗传修改的线虫体内找到了一个参与神经细胞发育的基因变异。
接着，科学家们检查了体内Sirtuin浓度已被提高的转基因果蝇——黑腹果蝇，此前研究表明，过度激活果蝇体内的Sirtuin会增加其寿命。杰姆斯团队制造出了一种具有更高Sirtuin浓度的新果蝇，但其并没有表现出长寿迹象。科学家们表示，遗传因子而非Sirtuin基因才是长寿的原因。
科学家们也合成出果蝇的Sirtuin来测试其能否被白藜芦醇所激活。然而，多方尝试之后，没有看到Sirtuin被白藜芦醇激活的现象。
最后，科学家们对缺乏Sirtuin基因的变异果蝇进行研究，发现节食仍然会增加其寿命。这表明，节食会通过激活Sirtuin来增加寿命这一论断不正确，节食与Sirtuin无关。
杰姆斯表示，所有研究都证明，Sirtuin同长寿无关，科学家们应专注于研究那些能控制衰老的过程。
生物探索推荐英文论文摘要：
Absence of effects of Sir2 overexpression on lifespan in C. elegans and Drosophila
Overexpression of sirtuins (NAD+-dependent protein deacetylases) has been reported to increase lifespan in budding yeast (Saccharomyces cerevisiae), Caenorhabditis elegans and Drosophila melanogaster. Studies of the effects of genes on ageing are vulnerable to confounding effects of genetic background. Here we re-examined the reported effects of sirtuin overexpression on ageing and found that standardization of genetic background and the use of appropriate controls abolished the apparent effects in both C. elegans and Drosophila. In C. elegans, outcrossing of a line with high-level sir-2.1 overexpression abrogated the longevity increase, but did not abrogate sir-2.1 overexpression. Instead, longevity co-segregated with a second-site mutation affecting sensory neurons. Outcrossing of a line with low-copy-number sir-2.1 overexpression also abrogated longevity. A Drosophila strain with ubiquitous overexpression of dSir2 using the UAS-GAL4 system was long-lived relative to wild-type controls, as previously reported3, but was not long-lived relative to the appropriate transgenic controls, and nor was a new line with stronger overexpression of dSir2. These findings underscore the importance of controlling for genetic background and for the mutagenic effects of transgene insertions in studies of genetic effects on lifespan. The life-extending effect of dietary restriction on ageing in Drosophila has also been reported to be dSir2 dependent. We found that dietary restriction increased fly lifespan independently of dSir2. Our findings do not rule out a role for sirtuins in determination of metazoan lifespan, but they do cast doubt on the robustness of the previously reported effects of sirtuins on lifespan in C. elegans and Drosophila.
