Live fast--live long? A commentary on a recent paper by Speakman et al.
Live fast--live long? A commentary on a recent paper by Speakman et al.
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活得快——活得长久？
DOI：
10.1111/j.1474-9728.2004.00113.x
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发表时间：
2004
期刊：
影响因子：
7.8
通讯作者：
VanVoorhies,WayneA
中科院分区：
文献类型：
--
作者：
VanVoorhies,WayneA
Speakman 等人 (2004) 最近发表的论文“解偶联和生存：高代谢的个体小鼠线粒体解偶联程度更高，寿命更长”，其意义重大有两个原因。首先，斯派克曼等人。证明在一组小鼠中，代谢率和寿命之间存在正相关。这一结果与长期以来提出的衰老理论相反，该理论将能量消耗与衰老成反比。其次，他们为为什么可能存在这种正相关性提供了可信的解释：解偶联蛋白激活的增加可能会提高代谢率，但会降低活性氧（ROS）的总体产生。因此，这项研究可能为理解和减缓衰老做出重要贡献。衰老与能量消耗率成反比这一概念的科学起源可以追溯到近 100 年前。 1908 年，鲁布纳发表了比较五种哺乳动物代谢率的结果，并得出结论，尽管它们的寿命存在很大差异，但这些哺乳动物的终生能量输出大致相同，具有质量特异性（代谢输出标准化为给定的体重）。珀尔对这些研究进行了扩展，他提出了“生存率假说”，该假说将有机体的代谢输出与其寿命直接联系起来（Pearl，1928）。连接这两者的因果机制尚不清楚，但 Pearl 提出，生命的持续时间是由重要细胞成分的消耗决定的，该细胞成分的消耗速度与代谢率成正比，耗尽后就会发生死亡。Harman (1956) 在提出有氧呼吸过程中产生自由基时，对连接代谢率和寿命的因果机制提出了更现代的解释。 负责代谢率和寿命之间的联系。根据这一假说（通常称为衰老的自由基理论），衰老是由自由基的产生引起的生物损伤累积的结果。这些自由基
The recent paper by Speakman et al.(2004),‘Uncoupled and surviving: individual mice with high metabolism have greater mitochondrial uncoupling and live longer’, is significant for two reasons. First, Speakman et al. demonstrate that within a cohort of mice there is a positive correlation between metabolic rate and longevity. This result is contrary to long-proposed theories of aging that inversely link energy expenditure to aging. Second, they provide a credible explanation for why such a positive correlation might exist: increased activation of uncoupling proteins may increase metabolic rates, but decrease the overall production of reactive oxygen species (ROS). As such, this research potentially provides an important contribution towards understanding and attenuating aging. The scientific origins of the concept that aging is inversely related to the rate of energy expenditure extend back nearly 100 years. In 1908 Rubner published results comparing metabolic rates in five species of mammals and concluded that despite large differences in their chronological longevity, these mammals had approximately equal, mass-specific (metabolic output standardized to a given body mass), lifetime energy output. These studies were expanded on by Pearl, who proposed the ‘rate of living hypothesis’, which directly linked the metabolic output of an organism to its longevity (Pearl, 1928). The causal mechanism linking these two was unclear, but Pearl proposed that the duration of life was determined by the exhaustion of a vital cellular component that was consumed at a rate proportional to the metabolic rate, with death occurring upon its depletion.Harman (1956) formulated a more modern interpretation of causal mechanisms linking metabolic rate and longevity when he proposed that free radicals produced during aerobic respiration were responsible for the link between metabolic rate and longevity. By this hypothesis, often called the free radical theory of aging, aging results from the accumulation of biological damage caused by the production of free radicals. These free radicals