Dietary restriction in long-lived dwarf flies
Dietary restriction in long-lived dwarf flies
复制标题
DOI：
10.1126/science.1069366
复制
发表时间：
2002-04-12
期刊：
影响因子：
56.9
通讯作者：
Partridge, L
中科院分区：
文献类型：
--
作者：
Clancy, DJ;Gems, D;Partridge, L
减缓衰老的干预措施为了解其原因提供了宝贵的见解。但它们是基于共同的潜在机制起作用的吗？最近对一种长寿的突变小鼠Ames侏儒的研究表明，通过另一种干预，即饮食限制，可以进一步延长其寿命，即将食物摄入量限制在自愿水平的70%左右(1)。这一发现表明，Ames突变和饮食限制通过不同的机制延缓衰老，因为Ames突变和饮食限制并不掩盖彼此对寿命的影响。使用果蝇，我们在这里表明：(1)通过胰岛素/胰岛素样生长因子（IGF）样信号通路（IIS）的突变和饮食限制通过重叠机制发生的衰老减缓；(2)必须通过至少一种正在研究的干预措施来最大化寿命，以适当地测试寿命延长机制不同的假设。减少IIS的突变延长了秀丽隐杆线虫和果蝇的寿命
Interventions that slow down aging provide invaluable insights into its causes. But do they act upon common underlying mechanisms? Recent work with a long-lived mutant mouse, the Ames dwarf, showed that its lifespan could be further extended by another intervention, dietary restriction, in which food intake was restricted to about 70% of voluntary levels (1). This finding was taken to demonstrate that the Ames mutation and dietary restriction slow aging by different mechanisms, because the Ames mutation and dietary restriction do not mask each other’s effect on life-span. Using the fruit fly Drosophila, we show here that (i) slowing of aging by a mutation in an insulin/insulin-like growth factor (IGF)–like signaling (IIS) pathway and by dietary restriction occurs by overlapping mechanisms and (ii) life-span must be maximized by at least one of the interventions under investigation for a proper test of the hypothesis that the mechanisms of life-span extension differ. Mutations that reduce IIS extend life-span in the nematode worm Caenorhabditis elegans and the fruit fly