法国国家科研中心研究人员1月28日报告说，他们通过实验发现，控制线虫的饮食可以大大延长这种生物的寿命。这一发现对哺乳动物也有借鉴意义。
研究人员在英国最新一期《衰老细胞》（Aging Cell）杂志上介绍说，无论是人还是动物，其寿命的长短在很大程度上取决于周边环境和生活方式，其中饮食作用尤为重要。为此，他们以秀丽隐杆线虫为对象开展了研究。这种虫是一种科学实验中的常用蠕虫，生命周期仅为3天。
研究人员为线虫特制了一份食谱，在严格控制食量的同时，保证营养的全面和均衡。结果发现，线虫体内一种名为slcf-1的衰老基因的表达受到了抑制，并且它体内丙酮酸盐的水平也有所上升。在这两种因素的作用下，线虫的寿命得以延长。
研究人员接下来将对哺乳动物开展类似实验，以了解通过控制饮食延长寿命的方法是否也适用于哺乳动物。
原文出处：
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.
