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Caloric restriction as a mechanism mediating resistance to environmental disease.

It has been observed that susceptibility to many degenerative diseases increases concurrently with industrialization and rising living standards. Although epidemiologic studies suggest that specific environmental and dietary factors may be important, caloric intake alone (as reflected in body size)...

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Detalles Bibliográficos
Autores principales: Frame, L T, Hart, R W, Leakey, J E
Formato: Texto
Lenguaje:English
Publicado: 1998
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533299/
https://www.ncbi.nlm.nih.gov/pubmed/9539025
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author Frame, L T
Hart, R W
Leakey, J E
author_facet Frame, L T
Hart, R W
Leakey, J E
author_sort Frame, L T
collection PubMed
description It has been observed that susceptibility to many degenerative diseases increases concurrently with industrialization and rising living standards. Although epidemiologic studies suggest that specific environmental and dietary factors may be important, caloric intake alone (as reflected in body size) may account for much of the differential risk observed among diverse human populations. It has been suggested from animal studies that caloric intake may be the primary effector for many hormonal, metabolic, physiologic, and behavioral responses that coordinate reproductive strategy to apparent availability of food. When caloric intake is excessive, particularly at critical developmental stages, physiologic priorities are set for body growth and fecundity rather than for endurance and longevity. The converse occurs during periods of famine, thus increasing the probability that sufficient individuals survive to restore the population when conditions improve. Calorically restricted rodents have significantly longer reproductive and total life spans than their ad libitum-fed controls and exhibit a spectrum of biochemical and physiologic alterations that characterize their adaptation to reduced intake. These include reduced stature, hypercorticism in the absence of elevated adrenocorticotropic hormone levels, increased metabolic efficiency, decreased mitogenic response coupled with increased rates of apoptosis, reduced inflammatory response, induction of stress proteins and DNA repair enzymes, altered drug-metabolizing enzyme expression, and modified cell-mediated immune function. The overall profile of these changes is one of improved defense against environmental stress. This has been suggested as the mechanistic basis for the protective effects of low body weight on radiation and chemically induced cancers in experimental animals. It may also explain the significantly higher thresholds of acute toxicity observed when calorically restricted rodents are exposed to certain test compounds.
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spelling pubmed-15332992006-08-08 Caloric restriction as a mechanism mediating resistance to environmental disease. Frame, L T Hart, R W Leakey, J E Environ Health Perspect Research Article It has been observed that susceptibility to many degenerative diseases increases concurrently with industrialization and rising living standards. Although epidemiologic studies suggest that specific environmental and dietary factors may be important, caloric intake alone (as reflected in body size) may account for much of the differential risk observed among diverse human populations. It has been suggested from animal studies that caloric intake may be the primary effector for many hormonal, metabolic, physiologic, and behavioral responses that coordinate reproductive strategy to apparent availability of food. When caloric intake is excessive, particularly at critical developmental stages, physiologic priorities are set for body growth and fecundity rather than for endurance and longevity. The converse occurs during periods of famine, thus increasing the probability that sufficient individuals survive to restore the population when conditions improve. Calorically restricted rodents have significantly longer reproductive and total life spans than their ad libitum-fed controls and exhibit a spectrum of biochemical and physiologic alterations that characterize their adaptation to reduced intake. These include reduced stature, hypercorticism in the absence of elevated adrenocorticotropic hormone levels, increased metabolic efficiency, decreased mitogenic response coupled with increased rates of apoptosis, reduced inflammatory response, induction of stress proteins and DNA repair enzymes, altered drug-metabolizing enzyme expression, and modified cell-mediated immune function. The overall profile of these changes is one of improved defense against environmental stress. This has been suggested as the mechanistic basis for the protective effects of low body weight on radiation and chemically induced cancers in experimental animals. It may also explain the significantly higher thresholds of acute toxicity observed when calorically restricted rodents are exposed to certain test compounds. 1998-02 /pmc/articles/PMC1533299/ /pubmed/9539025 Text en
spellingShingle Research Article
Frame, L T
Hart, R W
Leakey, J E
Caloric restriction as a mechanism mediating resistance to environmental disease.
title Caloric restriction as a mechanism mediating resistance to environmental disease.
title_full Caloric restriction as a mechanism mediating resistance to environmental disease.
title_fullStr Caloric restriction as a mechanism mediating resistance to environmental disease.
title_full_unstemmed Caloric restriction as a mechanism mediating resistance to environmental disease.
title_short Caloric restriction as a mechanism mediating resistance to environmental disease.
title_sort caloric restriction as a mechanism mediating resistance to environmental disease.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533299/
https://www.ncbi.nlm.nih.gov/pubmed/9539025
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