Abstract
Subsequent to the slow historical development of the use of controlled feeding to extend maximum lifespan in rodents, interest is now focussed on exploring the potential of this animal model to understand more fully the mechanisms of aging and the biochemical etiology of chronic age-related pathologies. The use of diet to extend lifespan has so far been restricted to rodent species within the Mammals, but confirmation of the reproducibility of this effect has been reported in spite of widely differing experimental designs (Merry and Holehan, 1985a, 1985b). Controlled underfeeding such as to limit access to the normal diet so that the body weight of experimental animals is maintained at 50% of age-matched ad libitum fed rats is one of the simplest and most effective designs to delay the age at which the rate of mortality increases and results in a 36–66% extension of the maximum lifespan (Masoro et al., 1980; Merry and Holehan, 1979, 1981). Although the immediate postweaning period is not the only phase of the lifespan susceptible to the effects of underfeeding, treatments which are continued for a longer fraction of the postweaning lifespan generally have a greater effect on extending longevity. It is uncertain if the immediate postweaning period is more sensitive to the effects of underfeeding in terms of lifespan extension, but it is clear that nutrition intervention restricted to 49 days postweaning substantially reduces tumor incidence in later life (Ross and Bras, 1971).
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Merry, B.J., Holehan, A.M. (1985). The Endocrine Response to Dietary Restriction in the Rat. In: Woodhead, A.D., Blackett, A.D., Hollaender, A. (eds) Molecular Biology of Aging. Basic Life Sciences, vol 35. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-2218-2_6
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