Restriction of energy intake, energy expenditure, and aging

Jon J Ramsey, Mary Ellen Harper, Richard Weindruch

Research output: Contribution to journalArticle

160 Citations (Scopus)

Abstract

Energy restriction (ER), without malnutrition, increases maximum life span and retards the development of a broad array of pathophysiological changes in laboratory rodents. The mechanism responsible for the retardation of aging by ER is, however, unknown. One proposed explanation is a reduction in energy expenditure (EE). Reduced EE may increase life span by decreasing the number of oxygen molecules interacting with mitochondria, thereby lowering reactive oxygen species (ROS) production. As a step toward testing this hypothesis, it is important to determine the effect of ER on EE. Several whole-body, organ, and cellular studies have measured the influence of ER on EE. In general, whole-body studies have reported an acute decrease in mass-adjusted EE that disappears with long-term ER. Organ-specific studies have shown that decreases in EE of liver and gastrointestinal tract are primarily responsible for initial reductions in EE with ER. These data, however, do not determine whether cellular EE is altered with ER. Three major processes contributing to resting EE at the cellular level are mitochondrial proton leak, Na+-K+-ATPase activity, and protein turnover. Studies suggest that proton leak and Na+-K+-ATPase activity are decreased with ER, whereas protein turnover is either unchanged or slightly increased with ER. Thus, two of the three major processes contributing to resting EE at the cellular level may be decreased with ER. Although additional cellular measurements are needed, the current results suggest that a lowering of EE could be a mechanism for the action of ER. (C) 2000 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)946-968
Number of pages23
JournalFree Radical Biology and Medicine
Volume29
Issue number10
DOIs
StatePublished - Nov 15 2000
Externally publishedYes

Fingerprint

Energy Intake
Energy Metabolism
Aging of materials
Adenosine Triphosphatases
Protons
Mitochondria
Malnutrition
Liver
Gastrointestinal Tract
Rodentia
Reactive Oxygen Species
Proteins
Oxygen
Molecules

Keywords

  • Caloric restriction
  • Free radicals
  • Longevity
  • Mitochondria
  • Oxygen consumption
  • Reactive oxygen species

ASJC Scopus subject areas

  • Medicine(all)
  • Toxicology
  • Clinical Biochemistry

Cite this

Restriction of energy intake, energy expenditure, and aging. / Ramsey, Jon J; Harper, Mary Ellen; Weindruch, Richard.

In: Free Radical Biology and Medicine, Vol. 29, No. 10, 15.11.2000, p. 946-968.

Research output: Contribution to journalArticle

Ramsey, Jon J ; Harper, Mary Ellen ; Weindruch, Richard. / Restriction of energy intake, energy expenditure, and aging. In: Free Radical Biology and Medicine. 2000 ; Vol. 29, No. 10. pp. 946-968.
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