Caloric Restriction: Conservation of Cellular Replicative Capacity in Vitro Accompanies Life-Span Extension in Mice

1995 ◽  
Vol 217 (2) ◽  
pp. 309-316 ◽  
Author(s):  
William R. Pendergrass ◽  
Yi Li ◽  
DeZhao Jiang ◽  
R.G. Fei ◽  
Norman S. Wolf
1995 ◽  
Vol 217 (2) ◽  
pp. 317-323 ◽  
Author(s):  
Norman S. Wolf ◽  
Philip E. Penn ◽  
DeZhao Jiang ◽  
Rui Gao Fei ◽  
William R. Pendergrass

2007 ◽  
Vol 10 (2) ◽  
pp. 157-172 ◽  
Author(s):  
Magda Katsiki ◽  
Niki Chondrogianni ◽  
Ioanna Chinou ◽  
A. Jennifer Rivett ◽  
Efstathios S. Gonos

2003 ◽  
Vol 171 (6) ◽  
pp. 2912-2921 ◽  
Author(s):  
Marco W. J. Schreurs ◽  
Kirsten B. J. Scholten ◽  
Esther W. M. Kueter ◽  
Janneke J. Ruizendaal ◽  
Chris J. L. M. Meijer ◽  
...  

2004 ◽  
Vol 17 (2) ◽  
pp. 230-244 ◽  
Author(s):  
Matthias Bauer ◽  
Anne C. Hamm ◽  
Melanie Bonaus ◽  
Andrea Jacob ◽  
Jens Jaekel ◽  
...  

We have monitored global changes in gene expression in mouse liver in response to fasting and sugar-fed conditions using high-density microarrays. From ∼20,000 different genes, the significantly regulated ones were grouped into specific signaling and metabolic pathways. Striking changes in lipid signaling cascade, insulin and dehydroepiandrosterone (DHEA) hormonal pathways, urea cycle and S-adenosylmethionine-based methyl transfer systems, and cell apoptosis regulators were observed. Since these pathways have been implicated to play a role in the aging process, and since we observe significant overlap of genes regulated upon starvation with those regulated upon caloric restriction, our analysis suggests that starvation may elicit a stress response that is also elicited during caloric restriction. Therefore, many of the signaling and metabolic components regulated during fasting may be the same as those which mediate caloric restriction-dependent life-span extension.


2011 ◽  
Vol 43 (5) ◽  
pp. 823-833 ◽  
Author(s):  
Mikael Molin ◽  
Junsheng Yang ◽  
Sarah Hanzén ◽  
Michel B. Toledano ◽  
Jean Labarre ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Pitchapat Sunthonkun ◽  
Rinsai Palajai ◽  
Pichayada Somboon ◽  
Chua Lee Suan ◽  
Malyn Ungsurangsri ◽  
...  

AbstractBenefits of whole grains as dietary supplements and active ingredients in health products have been promoted. Despite being neglected as an agricultural byproduct of polished rice, pigmented rice bran has emerged as a promising source of natural anti-aging compounds. Indeed, the extract of red rice bran Hom Dang cultivar contained rich phenolic acids and flavonoids. It displayed high antioxidant activities in vitro and in vivo assays. Using yeast model, extract and bioactive compounds, quercetin and protocatechuic acid found in the rice bran pericarp, effectively reduced levels of intracellular reactive oxygen species (ROS), restored plasma membrane damages and prolonged life-span of pre-treated wild-yeast cells. Importantly, these molecules modulated life span-extension through a mechanism of ROS reduction that resembles to that operated under the highly conserved Tor1- and Sir2-dependent signaling pathways, with the human homologs TORC1 and SIRT1, respectively. The key longevity factors Sch9 and Rim15 kinases, Msn2/4 regulators and a novel transcription factor Asg1, the antioxidant enzymes superoxide dismutases and glutathione peroxidases played important role in mediating longevity. Yeast clearly provides an instrumental platform for rapid screening of compounds with anti-aging efficacies and advances knowledge in the molecular study of ageing.


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