The effect of long‐term food restriction on tumours in rodents

Tucker, Mary J.

doi:10.1002/ijc.2910230611

Cited by 178 publications

(55 citation statements)

References 9 publications

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“…From these experiments, it was believed that life extension in these GF animals may be characterized by a infectious disease-free status. Data from the second aspect of our experiment agrees with other studies indicating that appropriate food restriction in rodents can increase mean and maximum life spans [1,2,5,8,10,[12][13][14]16,19,[21][22][23].…”

Section: Disussionsupporting

confidence: 91%

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Effects of Germfree Status and Food Restriction on Longevity and Growth of Mice

Tazume

Umehara

Matsuzawa

et al. 1991

Experimental Animals

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An investigation was undertaken to study the effects of germfree (GF) status and mild food restriction on life span in GF and specific pathogen-free (SPF) male ICR mice either full-fed (ad libitum) or on a restricted diet of 4.5 grams per day (equivalent to approximately 80% of full-fed intake) from five-week-old. The mean life span of the full-fed SPF and GF mice was 75.9 and 88.9 weeks respectively, whie the mean life span of the food-restricted SPF and GF mice was 117.5 and 109.6 weeks, respectively. Mice in both GF and SPF food-restricted groups were characterized by lower body weight and increased survival. These findings suggest that the cessation of growth may be importantly and perhaps causally related to longevity. The GF mice survived longer than the SPF mice, but the combination of GF status with food restriction did not seem to extend life span more than food restriction alone.

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Section: Disussionsupporting

confidence: 91%

“…McCay et al [8] has reported that restric ling the food intake of rats markedly increased life span. Since then, many repetitions of similarly designed experiments have confirmed this fact [1,2,5,10,13,14,16,19,. It therfore appears that food restriction influences basic mechanisms of the aging process common to these animals.…”

mentioning

confidence: 93%

Effects of Germfree Status and Food Restriction on Longevity and Growth of Mice

Tazume

Umehara

Matsuzawa

et al. 1991

Experimental Animals

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“…Rather, it is the complex interactions of the environment and diet (total caloric intake) with the SD rat's genome that produces or prevents the polygenic phenotype of diabesity from being expressed. It also appears that feeding modified diets with lowered protein, reduced metabolizable energy content, and increased fiber does not necessarily result in the control of diabesity or improved survival if the diets are provided ad libitum (Tucker, 1979;Iwasaki et al, 1988;Masoro et al, 1989;Keenan et al, 1994aKeenan et al, , 1994bKeenan et al, , 1995aKeenan et al, , 1995bKeenan et al, , 2000aKeenan et al, , 2000bRoe et al, 1995;Yu, 1995;Masoro, 1996;Whitaker et al, 1997;Masoro et al, 1996). Only dietary restriction (DR) of all diets tested in rodents consistently improves survival and delays the onset of the spontaneous development of obesity and the degenerative diseases referred to as "diabesity.…”

Section: Discussionmentioning

confidence: 99%

Diabesity: A Polygenic Model of Dietary-Induced Obesity from Ad Libitum Overfeeding of Sprague–Dawley Rats and Its Modulation by Moderate and Marked Dietary Restriction

et al. 2005

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This study compared the effects of ad libitum (AL) overfeeding and moderate or marked dietary restriction (DR) on the pathogenesis of a metabolic syndrome of diabesity comprised of age-related degenerative diseases and obesity in a outbred stock of Sprague-Dawley (SD) rats [Crl:CD (SD) IGS BR]. SD rats were fed Purina Certified Rodent Diet AL (group 1), DR at 72-79% of AL (group 2), DR at 68-72% of AL (group 3) or DR at 47-48% of AL (group 4) for 106 weeks. Interim necropsies were performed at 13, 26, and 53 weeks, after a 7-day 5-bromo-2-deoxyuridine (BrdU)-filled minipump implantation. Body weights, organ weights, carcass analysis, in-life data including estrous cyclicity, and histopathology were determined. At 6-7 weeks of age SD rats had 6% body fat. AL-feeding resulted in hypertriglyceridemia, hypercholesterolemia, and dietary-induced obesity (DIO) by study week 14, with 25% body fat that progressed to 36-42% body fat by 106 weeks. As early as 14 weeks, key biomarkers developed for spontaneous nephropathy, cardiomyopathy, and degenerative changes in multiple organ systems. Early endocrine disruption was indicated by changes in metabolic and endocrine profiles and the early development and progression of lesions in the pituitary, pancreatic islets, adrenals, thyroids, parathyroids, liver, kidneys, and other tissues. Reproductive senescence was seen by 9 months with declines in estrous cyclicity and pathological changes in the reproductive organs of both sexes fed AL or moderate DR, but not marked DR. The diabesity syndrome in AL-fed, DIO SD rats was readily modulated or prevented by moderate to marked DR. Moderate DR of balanced diets resulted in a better toxicology model by significantly improving survival, controlling adult body weight and obesity, reducing the onset, severity, and morbidity of age-related renal, endocrine, metabolic, and cardiac diseases. Moderate DR feeding reduces study-to-study variability, increases treatment exposure time, and increases the ability to distinguish true treatment effects from spontaneous aging. The structural and metabolic differences between the phenotypes of DIO and DR SD rats indicated changes of polygenic expression over time in this outbred stock. AL-overfeeding of SD rats produces a needed model of DIO and diabesity that needs further study of its patterns of polygenic expression and phenotype.

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“…DR delays the time of occurrence of various age-associated diseases, including cancer (22)(23)(24), and is a useful modulator of chemical toxicity. However, its mode of action remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Hepatic nuclear ploidy distribution of dietary-restricted mice.

Lü

Hinson

et al. 1993

Environ Health Perspect

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Hepatic parenchymal cells in most adult mammals are polyploid, with most of the cells in the quiescent or low-proliferation state. Polyploidization has been related to carcinogenesis and aging, and both end points are significantly affected by dietary restriction (DR). Direct measures of hepatic nuclear polyploidization in DR B6C3F, mice have not been examined. We examined the effect of DR on distributions of nuclear ploidy in both sexes and on different age groups of R6C3F, mice. Differences between young and old male mice and between old male and female mice were also compared. Hepatic nuclear ploidy values were measured by flow cytometry. The DNA histograms were analyzed for the percentage of nuclei having different classes of DNA content by gating channels between the areas under the peaks of diploid, tetraploid, and octaploid. The results indicate that 1 or 26 months of DR started at 4 months of age did not alter hepatic nuclear ploidy distributions in young and old mice. Our data suggest that in the male mouse, polyploidization is established by 5 months of age for hepatic nuclei and that ploidy classes are affected by sex at 30 months of age. For females, effects in the octaploid nuclei are seen as a result of DR.

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The effect of long‐term food restriction on tumours in rodents

Cited by 178 publications

References 9 publications

Effects of Germfree Status and Food Restriction on Longevity and Growth of Mice

Effects of Germfree Status and Food Restriction on Longevity and Growth of Mice

Diabesity: A Polygenic Model of Dietary-Induced Obesity from Ad Libitum Overfeeding of Sprague–Dawley Rats and Its Modulation by Moderate and Marked Dietary Restriction

Hepatic nuclear ploidy distribution of dietary-restricted mice.

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