法國國家科研中心研究人員1月28日報告說,，他們通過實驗發(fā)現(xiàn),，控制線蟲的飲食可以大大延長這種生物的壽命。這一發(fā)現(xiàn)對哺乳動物也有借鑒意義,。
研究人員在英國最新一期《衰老細(xì)胞》（Aging Cell）雜志上介紹說,，無論是人還是動物，其壽命的長短在很大程度上取決于周邊環(huán)境和生活方式,，其中飲食作用尤為重要,。為此，他們以秀麗隱桿線蟲為對象開展了研究,。這種蟲是一種科學(xué)實驗中的常用蠕蟲,，生命周期僅為3天。
研究人員為線蟲特制了一份食譜,，在嚴(yán)格控制食量的同時,，保證營養(yǎng)的全面和均衡。結(jié)果發(fā)現(xiàn),，線蟲體內(nèi)一種名為slcf-1的衰老基因的表達(dá)受到了抑制,，并且它體內(nèi)丙酮酸鹽的水平也有所上升。在這兩種因素的作用下,，線蟲的壽命得以延長,。
研究人員接下來將對哺乳動物開展類似實驗，以了解通過控制飲食延長壽命的方法是否也適用于哺乳動物,。
原文出處：
Aging Cell DOI: 10.1111/j.1474-9726.2010.00640.x
Pyruvate imbalance mediates metabolic reprogramming and mimics lifespan extension by dietary restriction in Caenorhabditis elegans
Laurent Mouchiroud1, Laurent Molin1, Prasad Kasturi1, Mohamed N. Triba2, Marc Emmanuel Dumas2, Marieangela C. Wilson3, Andrew P. Halestrap3, Damien Roussel4, Ingrid Masse1, Nicolas Dallière1, Laurent Ségalat?, Marc Billaud1, Florence Solari1
Summary
Dietary restriction (DR) is the most universal intervention known to extend animal lifespan. DR also prevents tumor development in mammals, and this effect requires the tumor suppressor PTEN. However, the metabolic and cellular processes that underly the beneficial effects of DR are poorly understood. We identified slcf-1 in an RNAi screen for genes that extend Caenorhabditis elegans lifespan in a PTEN/daf-18-dependent manner. We showed that slcf-1 mutation, which increases average lifespan by 40%, mimics DR in worms fed ad libitum. An NMR-based metabolomic characterization of slcf-1 mutants revealed lower lipid levels compared to wild-type animals, as expected for dietary-restricted animals, but also higher pyruvate content. Epistasis experiments and metabolic measurements support a model in which the long lifespan of slcf-1 mutants relies on increased mitochondrial pyruvate metabolism coupled to an adaptive response to oxidative stress. This response requires DAF-18/PTEN and the previously identified DR effectors PHA-4/FOXA, HSF-1/HSF1, SIR-2.1/SIRT-1, and AMPK/AAK-2. Overall, our data show that pyruvate homeostasis plays a central role in lifespan control in C. elegans and that the beneficial effects of DR results from a hormetic mechanism involving the mitochondria. Analysis of the SLCF-1 protein sequence predicts that slcf-1 encodes a plasma membrane transporter belonging to the conserved monocarboxylate transporter family. These findings suggest that inhibition of this transporter homolog in mammals might also promote a DR response.
