Life Span Study of SPF Fischer 344 Male Rats Fed AdLibitum or Restricted Diets: Longevity, Growth, Lean Body Mass and Disease

Yu, Byung Pal; Masoro, Edward J.; Murata, Ikuo; Bertrand, Helen A.; Lynd, Frederick T.

doi:10.1093/geronj/37.2.130

Cited by 545 publications

(177 citation statements)

References 12 publications

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“…In conclusion, the present findings document that dietary restriction is capable of a positive modulation of the synaptic dynamic morphology which may be due to the many reported effects of a reduced caloric intake on free radical generation and/or control (4,6,7,(35)(36)(37)(38)(39)41).…”

Section: Discussionsupporting

confidence: 61%

“…Despite many hypotheses, so far all have failed to explain the mechanism of action of different food restriction schedules, it remains well proven that the function organ systems are better and longer preserved in dietary restricted animals. Namely, the immunological response is markedly improved (4), renal and myocardial diseases (5) as well as the incidence of tumor mediated by free radicals (6,7) are reduced in food restricted animals.…”

Section: Introductionmentioning

confidence: 99%

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Dietary restriction modulates synaptic structural dynamics in the aging hippocampus

Bertoni–Freddari

Fattoretti

Caselli

et al. 1999

AGE

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A computer-assisted morphometric study has been carried out on the synaptic ultrastructural features in the hippocampus of 14-month old (DR14) and 27-month old (DR27) dietary restricted (-50% lipids and -35% carbohydrates) rats. Age-matched controls were maintained on an ad libitum (AL) feeding schedule. Synaptic numeric density (Nv), surface density (Sv) and average area (S) were the parameters measured. In old AL vs. adult AL animals, Nv decreased to a not significant extent, while S increased and Sv decreased significantly. In DR14 rats vs. AL littermates Nv increased significantly, but S and Sv were unchanged. DR27 rats vs. agematched AL controls showed a significant increase of Nv and Sv while S was significantly decreased. Comparing DR14 vs. DR27, no significant difference due to age was documented. Both in DR14 and in DR27 groups the percent distribution of S showed a marked increase of smaller contact zones. Despite reporting on discrete aspects of synaptic ultrastructure, Nv and S are supported to be in an inverse relationship which aims at maintaining Sv constant. Thus, these three ultrastructural parameters when taken together per experimental group, appear to provide information on synaptic morphological rearrangements. In this context, the percent increase of smaller synapses in DR animals is consistent with the idea of a marked remodelling process. Considering previous data from the same groups of rats reporting significant changes in neuronal membrane lipid composition and fluidity, we interpret our findings to account for a positive modulation of dietary restriction on the synaptic structural dynamics.

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Section: Discussionsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 99%

Dietary restriction modulates synaptic structural dynamics in the aging hippocampus

Bertoni–Freddari

Fattoretti

Caselli

et al. 1999

AGE

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“…In general, the daily caloric intake subjected to CR has been restricted to 50% to 70% of the average food intake in subjects eating ad libitum [1,2] . CR was first reported to retard aging and prolong median and maximal life span in the 1930s [3] .…”

mentioning

confidence: 99%

Caloric restriction and heart function: is there a sensible link?

Han

Ren

2010

Acta Pharmacol Sin

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Calorie restriction (CR) is defined as a reduction in calorie intake below the usual ad libitum intake without malnutrition. In general, the daily caloric intake subjected to CR has been restricted to 50% to 70% of the average food intake in subjects eating ad libitum [1,2] . CR was first reported to retard aging and prolong median and maximal life span in the 1930s [3] . Over the last several decades, CR has been widely studied which exhibits an apparent beneficial impact on longevity, ageassociated diseases, and attenuation of functional decline, across a broad variety of species (including rats, mice, fish, flies, worms and yeast) [4,5] . Moreover, CR provides protection against a cadre of chronic diseases including diabetes mellitus, neurodegenerative diseases, autoimmune disorders [6][7][8] and cancer [9][10][11][12] . CR has been shown to alter a variety of physiological parameters especially reduced metabolic rate and oxidative damage, resulting in a decrease in the incidence of cardiovascular diseases [13] . In response to energy deficiency, experimental animals experience a drastic decrease in both fat mass and lean body mass. Muscle mass is overtly reduced, although the rate of loss of function and mass/body weight with the aging process is attenuated [9,[14][15][16] . Metabolic rate may decrease transiently although studies have indicated similar metabolic rate per kg lean body mass to that of ad libitum fed rodents in longterm CR protocol [17] . Body temperature, systolic and diastolic blood pressure all decrease [18,19] along with the reduced sympathetic activity [20] . CR-treated animals are more spontaneously active and display superior cognitive abilities compared to their ad libitum counterparts [21,22] .The most prominent mechanism that may be responsible for the beneficial health and physiological effects of CR are usually mediated through increased insulin sensitivity which results in reduced plasma glucose and insulin concentrations and improved glucose tolerance [23] ; reduced levels of oxidative stress (decreased oxidative damage to proteins, lipids and DNA) [24] , increased resistance to various types of stress including heat, oxidative and metabolic stress [25] as well as enhanced immune function [26] . Impact of CR on agingAn inverse relationship between calorie intake and lifespan has been revealed in mice, suggesting a key role for regulators of energy metabolism in the mechanism of CR. Accordingly, CR-induced metabolic reprogramming may be a key event in the mechanism of lifespan extension [27,28] . The age when CR is started, the severity of restriction, and strain or genetic background of animals determine the magnitude of life extension. The only mammals in which CR has clearly been shown ReviewCaloric restriction and heart function: is there a sensible link? Calorie restriction (CR) is defined as a reduction in calorie intake below the usual ad libitum intake without malnutrition. Ample of clinical and experimental evidence has demonstrated that CR is capable of retarding aging p...

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“…Consistent with it are the increase in life span upon food restriction [18,19] and the high levels of antioxidants in humans which may have facilitated the evolution of man's longevity [20][21][22][23]. The important factor responsible for longevity appears to be the basal metabolic rate [24,25], i.e.…”

mentioning

confidence: 99%

Do mitochondrial DNA fragments promote cancer and aging?

Richter

1988

FEBS Letters

211

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Reactive oxygen species are important in carcinogenesis, diseases, and aging, probably through oxidative damage of DNA. Our understanding of this relationship at the molecular level is very sketchy. It has recently been found that in mitochondria oxidative DNA damage is particularly high and may not be repaired efficiently. I propose that oxidatively generated DNA fragments escape from mitochondria and become integrated into the nuclear genome. This may transform cells to a cancerous state. Time‐dependent nuclear accumulation of mitochondrial DNA fragments may progressively change the nuclear information content and thereby cause aging. This proposal can be tested experimentally.

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Life Span Study of SPF Fischer 344 Male Rats Fed AdLibitum or Restricted Diets: Longevity, Growth, Lean Body Mass and Disease

Cited by 545 publications

References 12 publications

Dietary restriction modulates synaptic structural dynamics in the aging hippocampus

Dietary restriction modulates synaptic structural dynamics in the aging hippocampus

Caloric restriction and heart function: is there a sensible link?

Do mitochondrial DNA fragments promote cancer and aging?

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