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能量消耗与衰老。

Energy expenditure and aging.

机构信息

University of Florida, Institute on Aging, Department of Aging and Geriatric Research, 210 E Mowry Rd, PO Box 112610, Gainesville, FL 32611-2610, United States.

出版信息

Ageing Res Rev. 2010 Jan;9(1):1-11. doi: 10.1016/j.arr.2009.08.002. Epub 2009 Aug 19.

Abstract

The study of energy expenditure (EE) has deep roots in understanding aging and lifespan in all species. In humans, total EE decreases substantially in advanced age resulting from parallel changes in resting metabolic rate (RMR) and activity EE. For RMR, this reduction appears to be due to a reduction in organ mass and specific metabolic rates of individual tissues. However, these anatomical changes explain very little regarding the decline in activity EE, which is governed by both genetic and environmental sources. The biological control centers for activity EE are closely coupled with body mass fluctuations and seem to originate in the brain. Several candidate neuromodulators may be involved in the age-related reduction of activity EE that include: orexin, agouti-related proteins and dopaminergic pathways. Unfortunately, the existing body of research has primarily focused on how neuromodulators influence weight gain and only a few studies have been performed in aging models. Recent evidence suggests that activity EE has an important role in dictating lifespan and thus places emphasis on future research to uncover the underlying biological mechanisms. The study of EE continues to unlock clues to aging.

摘要

能量消耗(EE)的研究在理解所有物种的衰老和寿命方面有着深厚的渊源。在人类中,由于静息代谢率(RMR)和活动 EE 的平行变化,总 EE 在高龄时会大幅下降。对于 RMR,这种减少似乎是由于器官质量和个别组织的特定代谢率的降低所致。然而,这些解剖结构的变化对于活动 EE 的下降解释得很少,活动 EE 受到遗传和环境因素的共同控制。活动 EE 的生物学控制中心与体重波动密切相关,似乎起源于大脑。几种候选神经调质可能参与了与年龄相关的活动 EE 减少,包括:食欲素、肥胖相关蛋白和多巴胺能途径。不幸的是,现有的研究主要集中在神经调质如何影响体重增加,只有少数研究在衰老模型中进行。最近的证据表明,活动 EE 在决定寿命方面起着重要作用,因此强调未来的研究以揭示潜在的生物学机制。EE 的研究继续为衰老提供线索。

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