生物谷报道：限制几个卡路里的热量就可以延长实验鼠和其他物种的寿命，但限制进食何以能够延长寿命仍然是一个谜。现在，研究人员终于在用于衰老研究的模型生物线虫（C. elegans）身上发现了限制热量与长寿命之间的特定联系。Nicholas Bishop 和 Leonard Guarente发现，限制饮食能激活头部ASI神经元中的转录因子SKN-1，后者然后会向周围组织发出增加代谢活性的信号。这种神经细胞影响非神经组织的现象表明，内分泌系统参与了其中。Panowski等人报告，小肠和头部及尾部少数细胞中一种名叫PHA-4的转录因子活性的增加也是由限制饮食所产生的寿命延长所必需的。PHA-4与哺乳动物体内的Foxa转录因子类似，后者影响发育和调控空腹血糖素和葡萄糖水平。关于这种联系的知识让我们看到了用药物来模仿限制热量之好处的希望。
英文原文：
Nature 447, 545-549 (31 May 2007) | doi:10.1038/nature05904; Received 12 February 2007; Accepted 9 May 2007
Two neurons mediate diet-restriction-induced longevity in C. elegans
Nicholas A. Bishop1 & Leonard Guarente1
Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
Correspondence to: Leonard Guarente1 Correspondence and requests for materials should be addressed to L.G. (Email: leng@mit.edu).
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Abstract
Dietary restriction extends lifespan and retards age-related disease in many species and profoundly alters endocrine function in mammals. However, no causal role of any hormonal signal in diet-restricted longevity has been demonstrated. Here we show that increased longevity of diet-restricted Caenorhabditis elegans requires the transcription factor gene skn-1 acting in the ASIs, a pair of neurons in the head. Dietary restriction activates skn-1 in these two neurons, which signals peripheral tissues to increase metabolic activity. These findings demonstrate that increased lifespan in a diet-restricted metazoan depends on cell non-autonomous signalling from central neuronal cells to non-neuronal body tissues, and suggest that the ASI neurons mediate diet-restriction-induced longevity by an endocrine mechanism.
