The Journal of Nutrition: Retarded Growth, Life Span, Ultimate Body Size and Age Changes in the Albino Rat After Feeding Diets Restricted in Calories

McCay, C. M.; Maynard, L. A.; Sperling, G.; Barnes, LeRoy L.

doi:10.1111/j.1753-4887.1975.tb05227.x

Cited by 62 publications

(20 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It was assumed that low birth weight babies were physiologically compromised by the mothers’ poor nutritional state at conception with further deleterious effects on foetal growth and development. This amplified the original McCance and Widdowson's experiments in pigs and McCay's studies on rats and dogs showing early food restriction induced permanent effects on the offspring's body size, metabolism, ageing and chronic diseases, which could not be rectified by the later provision of adequate nutrients . Hales showed experimentally that protein deficiency compromised the development of the pancreas's capacity for insulin production and the liver's structure and function .…”

Section: Maternal Diet and Epigenetic Programming In Early Developmenmentioning

confidence: 84%

Emerging concepts on the role of epigenetics in the relationships between nutrition and health

2018

View full text Add to dashboard Cite

Understanding the physiological and metabolic underpinnings that confer individual differences in responses to diet and diet-related chronic disease is essential to advance the field of nutrition. This includes elucidating the differences in gene expression that are mediated through programming of the genome through epigenetic chromatin modifications. Epigenetic landscapes are influenced by age, genetics, toxins and other environmental factors, including dietary exposures and nutritional status. Epigenetic modifications influence transcription and genome stability are established during development with life-long consequences. They can be inherited from one generation to the next. The covalent modifications of chromatin, which include methylation and acetylation, on DNA nucleotide bases, histone proteins and RNA are derived from intermediates of one-carbon metabolism and central metabolism. They influence key physiological processes throughout life, and together with inherited DNA primary sequence, contribute to responsiveness to environmental stresses, diet and risk for age-related chronic disease. Revealing diet-epigenetic relationships has the potential to transform nutrition science by increasing our fundamental understanding of: (i) the role of nutrients in biological systems, (ii) the resilience of living organisms in responding to environmental perturbations, and (iii) the development of dietary patterns that programme physiology for life-long health. Epigenetics may also enable the classification of individuals with chronic disease for specific dietary management and/or for efficacious diet-pharmaceutical combination therapies. These new emerging concepts at the interface of nutrition and epigenetics were discussed, and future research needs identified by leading experts at the 26th Marabou Symposium entitled 'Nutrition, Epigenetics, Genetics: Impact on Health and Disease'. For a compilation of the general discussion at the marabou symposium, click here http://www.marabousymposium.org/.

show abstract

Section: Maternal Diet and Epigenetic Programming In Early Developmenmentioning

confidence: 84%

Emerging concepts on the role of epigenetics in the relationships between nutrition and health

2018

View full text Add to dashboard Cite

show abstract

“…Caloric restriction, methionine restriction and rapamycin addition were the few interventions that truly prolong the lifespans of vertebrates (40–42). Other interventions such as resveratrol, metformin and sirtuin activators were also reported to extend mouse lifespans (39).…”

Section: Discussionmentioning

confidence: 99%

Spermidine Prolongs Lifespan and Prevents Liver Fibrosis and Hepatocellular Carcinoma by Activating MAP1S-Mediated Autophagy

et al. 2017

View full text Add to dashboard Cite

Liver fibrosis and hepatocellular carcinoma (HCC) have worldwide impact but continue to lack safe, low cost and effective treatments. In this study, we show how the simple polyamine spermidine can relieve cancer cell defects in autophagy which trigger oxidative stress-induced cell death and promote liver fibrosis and HCC. We found that the autophagic marker protein LC3 interacted with the microtubule-associated protein MAP1S which positively regulated autophagy flux in cells. MAP1S stability was regulated in turn by its interaction with the histone deacetylase HDAC4. Notably, MAP1S-deficient mice exhibited a 20% reduction in median survival and developed severe liver fibrosis and HCC under stress. Wild-type mice or cells treated with spermidine exhibited a relative increase in MAP1S stability and autophagy signaling via depletion of cytosolic HDAC4. Extending recent evidence that orally administered spermidine can extend lifespan in mice, we determined that life extension of up to 25% can be produced by lifelong administration which also reduced liver fibrosis and HCC foci as induced by chemical insults. Genetic investigations established that these observed impacts of oral spermidine administration relied upon MAP1S-mediated autophagy. Our findings offer a preclinical proof of concept for the administration of oral spermidine to prevent liver fibrosis and HCC and potentially extend lifespan.

show abstract

“…The diet known as calorie restriction (CR) prolongs the lifespan of numerous species, including fungi, invertebrates, and mammals [1,12,13]. Whether or not Sir2p enzymes play a role in CR-mediated lifespan extension is hotly debated.…”

Section: Introductionmentioning

confidence: 99%

MSN2 and MSN4 Link Calorie Restriction and TOR to Sirtuin-Mediated Lifespan Extension in Saccharomyces cerevisiae

et al. 2007

View full text Add to dashboard Cite

Calorie restriction (CR) robustly extends the lifespan of numerous species. In the yeast Saccharomyces cerevisiae, CR has been proposed to extend lifespan by boosting the activity of sirtuin deacetylases, thereby suppressing the formation of toxic repetitive ribosomal DNA (rDNA) circles. An alternative theory is that CR works by suppressing the TOR (target of rapamycin) signaling pathway, which extends lifespan via mechanisms that are unknown but thought to be independent of sirtuins. Here we show that TOR inhibition extends lifespan by the same mechanism as CR: by increasing Sir2p activity and stabilizing the rDNA locus. Further, we show that rDNA stabilization and lifespan extension by both CR and TOR signaling is due to the relocalization of the transcription factors Msn2p and Msn4p from the cytoplasm to the nucleus, where they increase expression of the nicotinamidase gene PNC1. These findings suggest that TOR and sirtuins may be part of the same longevity pathway in higher organisms, and that they may promote genomic stability during aging.

show abstract

The Journal of Nutrition: Retarded Growth, Life Span, Ultimate Body Size and Age Changes in the Albino Rat After Feeding Diets Restricted in Calories

Cited by 62 publications

References 0 publications

Emerging concepts on the role of epigenetics in the relationships between nutrition and health

Emerging concepts on the role of epigenetics in the relationships between nutrition and health

Spermidine Prolongs Lifespan and Prevents Liver Fibrosis and Hepatocellular Carcinoma by Activating MAP1S-Mediated Autophagy

MSN2 and MSN4 Link Calorie Restriction and TOR to Sirtuin-Mediated Lifespan Extension in Saccharomyces cerevisiae

Contact Info

Product

Resources

About