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Overview of caloric restriction and ageing
Abstract
It has been known for some 70 years that restricting the food intake of laboratory rats extends their mean and maximum life span. In addition, such life extension has been observed over the years in many other species, including mice, hamsters, dogs, fish, invertebrate animals, and yeast. Since this life-extending action appears to be due to a restricted intake of energy, this dietary manipulation is referred to as caloric restriction (CR). CR extends life by slowing and/or delaying the ageing processes. The underlying biological mechanism responsible for the life extension is still not known, although many hypotheses have been proposed. The Growth Retardation Hypothesis, the first proposed, has been tested and found wanting. Although there is strong evidence against the Reduction of Body Fat Hypothesis, efforts have recently been made to resurrect it. While the Reduction of Metabolic Rate Hypothesis is not supported by experimental findings, it nevertheless still has advocates. Currently, the most popular concept is the Oxidative Damage Attenuation Hypothesis; the results of several studies provide support for this hypothesis, while those of other studies do not. The Altered Glucose-Insulin System Hypothesis and the Alteration of the Growth Hormone-IGF-1 Axis Hypothesis have been gaining favor, and data have emerged that link these two hypotheses as one. Thus, it may now be more appropriate to refer to them as the Attenuation of Insulin-Like Signaling Hypothesis. Finally, th…
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Diet restriction and dwarf mutations extend lifespan in rodents.
“Beneficial effects of diet restriction (DR)21 and dwarf mutations, both of which extend lifespan in rodents, may to some degree result from repression of the mTOR complex 1 (mTORC1) pathway22,23.”
From Rapamycin fed late in life extends lifespan in genetically heterogeneous mice (2009) · cites this paper as [21]
In most reports, diet restriction produces little if any benefit if started after about 550 days of age.
“Our demonstration that rapamycin feeding increases lifespan even when started late in life, as well as the absence of changes in body weight (data not shown), distinguish our results from studies using DR; in all cases DR reduces body weight, and in most reports21, though not all24, DR produces little if any benefit if started after about 550 days of age.”
From Rapamycin fed late in life extends lifespan in genetically heterogeneous mice (2009) · cites this paper as [21]
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IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice
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Sirtuin activators mimic caloric restriction and delay ageing in metazoans
Wood, J. G., Rogina, B., Lavu, S., Howitz, K., Helfand, S. L., Tatar, M., & Sinclair, D. (2004) · Nature · doi:10.1038/nature02789 · Cited by 1,868
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Anderson, R. M., Bitterman, K. J., Wood, J. G., Medvedik, O., & Sinclair, D. A. (2003) · Nature · doi:10.1038/nature01578 · Cited by 736
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Metadata
- Authors
- Masoro, E. J.
- Venue
- Mechanisms of Ageing and Development
- Publisher
- Elsevier BV
- Published
- 2005-09
- Volume
- 126
- Issue
- 9
- Pages
- 913-922
- ISSN
- 0047-6374
- Cited by
- 879
- References
- 5
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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