近日由美国佛罗里达州斯克里普斯研究院的科学家领导的一个研究小组证实一条调控营养吸收和能量平衡生物信号可影响线虫寿命的长短。这一研究发现在线发布在5月12日的《自然》（Nature）杂志上。
“这是我们**次在线虫中鉴定出这些分子，并证实它们不仅可作为营养利用率的信号分子，并可*终影响线虫的寿命，”斯克里普斯研究院新陈代谢与老化系助理教授MatthewGill博士说：“值得关注的是，在人类及线虫中都存在这些相同的分子，因此这些分子极有可能在两种生物体中发挥了相似的作用。”
在这篇文章中，科研人员鉴定出的是一类来自脂质的信号作用分子称为N-酰基乙醇胺（N-acylethanolamines，NAEs)。过去的研究表明它能在哺乳动物中调控营养吸收和能量平衡。Gill及同事在新研究中证实节食可导致线虫中NAE的丰度显著下降，而仅仅NAE的缺乏就足以使得线虫寿命延长。
“众所周知当线虫处于节食状态时，它的寿命可延长40-50%。然而在新研究中我们惊奇地发现仅需要给予其中的一种NAE分子eicosapentaenoylethanolamide就可完全终止寿命的延长，”Gill说。
研究人员发现这种特异的NAE与哺乳动物中的内源性**素（endocannabinoid）非常相似。内源性**素可对多种不同的生理过程包括营养摄入和能量平衡、炎症以及神经功能起重要的调控作用。“现在我们在线虫中鉴别出了新型内源性**素系统的其他组分，从而为研究者们开展NAE与内源性**素的生理学研究提供了一个新的模式系统，”Gill说。
此外，研究人员还在新研究中确定了脂肪，NAE水平与寿命之间的联系。过去一些研究团体曾在啮齿动物中证实脂肪酸的利用率可影响NAE的水平。在新研究中Gill及同事们发现遗传工程修饰的线虫无法生成的某种多不饱和脂肪酸不仅与特异的NAEs水平下降有关，还可影响线虫的寿命。Gill表示新研究发现为推动科学家们开发出影响衰老及衰老相关**的**指明了新方向。
推荐原文摘要：N-acylethanolamine signalling mediates the effect of diet onlifespan in Caenorhabditis elegans
Dietary restriction is a robust means of extending *****lifespan and postponing age-related disease in many species,including yeast, nematode worms, flies and rodents1, 2. Studies ofthe genetic requirements for lifespan extension by dietaryrestriction in the nematode Caenorhabditis elegans have implicateda number of key molecules in this process3, 4, 5, including thenutrient-sensing target of rapamycin (TOR) pathway6 and the Foxatranscription factor PHA-4 (ref. 7). However, little is known aboutthe metabolic signals that coordinate the organismal response todietary restriction and maintain homeostasis when nutrients arelimited. The endocannabinoid system is an excellent candidate forsuch a role given its involvement in regulating nutrient intake andenergy balance8. Despite this, a direct role for endocannabinoidsignalling in dietary restriction or lifespan determination has yetto be demonstrated, in part due to the apparent absence ofendocannabinoid signalling pathways in model organisms that areamenable to lifespan analysis9. N-acylethanolamines (NAEs) arelipid-derived signalling molecules, which include the mammalianendocannabinoid arachidonoyl ethanolamide. Here we identify NAEs inC. elegans, show that NAE abundance is reduced under dietaryrestriction and that NAE deficiency is sufficient to extendlifespan through a dietary restriction mechanism requiring PHA-4.Conversely, dietary supplementation with the nematode NAEeicosapentaenoyl ethanolamide not only inhibitsdietary-restriction-induced lifespan extension in wild-type worms,but also suppresses lifespan extension in a TOR pathway mutant.This demonstrates a role for NAE signalling in ageing and indicatesthat NAEs represent a signal that coordinates nutrient status withmetabolic changes that ultimately determine lifespan.