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

1995 ◽  
Vol 217 (2) ◽  
pp. 317-323 ◽  
Author(s):  
Norman S. Wolf ◽  
Philip E. Penn ◽  
DeZhao Jiang ◽  
Rui Gao Fei ◽  
William R. Pendergrass
Keyword(s):  
Life Span ◽  
Caloric Restriction ◽  
Replicative Capacity ◽  
Life Span Extension

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
Keyword(s):  
Life Span ◽  
Caloric Restriction ◽  
Replicative Capacity ◽  
Life Span Extension

scholarly journals Caloric Restriction Extends Yeast Chronological Life Span by Optimizing the Snf1 (AMPK) Signaling Pathway

2017 ◽  
Vol 37 (13) ◽  
Author(s):  
Margaret B. Wierman ◽  
Nazif Maqani ◽  
Erika Strickler ◽  
Mingguang Li ◽  
Jeffrey S. Smith
Keyword(s):  
Transcription Factors ◽  
Life Span ◽  
Caloric Restriction ◽  
Atp Depletion ◽  
Model Organisms ◽  
Diauxic Shift ◽  
Acetyl Coa ◽  
Α Subunit ◽  
Chronological Life Span

ABSTRACT AMP-activated protein kinase (AMPK) and the homologous yeast SNF1 complex are key regulators of energy metabolism that counteract nutrient deficiency and ATP depletion by phosphorylating multiple enzymes and transcription factors that maintain energetic homeostasis. AMPK/SNF1 also promotes longevity in several model organisms, including yeast. Here we investigate the role of yeast SNF1 in mediating the extension of chronological life span (CLS) by caloric restriction (CR). We find that SNF1 activity is required throughout the transition of log phase to stationary phase (diauxic shift) for effective CLS extension. CR expands the period of maximal SNF1 activation beyond the diauxic shift, as indicated by Sak1-dependent T210 phosphorylation of the Snf1 catalytic α-subunit. A concomitant increase in ADP is consistent with SNF1 activation by ADP in vivo. Downstream of SNF1, the Cat8 and Adr1 transcription factors are required for full CR-induced CLS extension, implicating an alternative carbon source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis. Indeed, CR increased acetyl-CoA levels during the diauxic shift, along with expression of both acetyl-CoA synthetase genes ACS1 and ACS2. We conclude that CR maximizes Snf1 activity throughout and beyond the diauxic shift, thus optimizing the coordination of nucleocytosolic acetyl-CoA production with massive reorganization of the transcriptome and respiratory metabolism.

Starvation response in mouse liver shows strong correlation with life-span-prolonging processes

2004 ◽  
Vol 17 (2) ◽  
pp. 230-244 ◽  
Author(s):  
Matthias Bauer ◽  
Anne C. Hamm ◽  
Melanie Bonaus ◽  
Andrea Jacob ◽  
Jens Jaekel ◽  
...  
Keyword(s):  
Life Span ◽  
Caloric Restriction ◽  
Metabolic Pathways ◽  
Mouse Liver ◽  
Aging Process ◽  
Urea Cycle ◽  
Global Changes ◽  
Starvation Response ◽  
Life Span Extension ◽  
Methyl Transfer

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.

scholarly journals Life Span Extension and H2O2 Resistance Elicited by Caloric Restriction Require the Peroxiredoxin Tsa1 in Saccharomyces cerevisiae

2011 ◽  
Vol 43 (5) ◽  
pp. 823-833 ◽  
Author(s):  
Mikael Molin ◽  
Junsheng Yang ◽  
Sarah Hanzén ◽  
Michel B. Toledano ◽  
Jean Labarre ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Life Span ◽  
Caloric Restriction ◽  
Life Span Extension ◽  
H2o2 Resistance

scholarly journals Antidiabeticheskiy biguanid metforminkak geroprotektor i antikantserogen

2011 ◽  
Vol 8 (3) ◽  
pp. 18-24
Author(s):  
V N Anisimov
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Life Span ◽  
Insulin Receptor ◽  
Caloric Restriction ◽  
Calorie Restriction ◽  
Insulin Signaling ◽  
Life Span Extension ◽  
Priority Direction ◽  
Prevention Of Cancer

Growth hormone (GH)/insulin-like growth factor 1 (IGF-1)/insulin, DAF-2 and insulin-receptor control life span in various species including human. It is possible that the life-prolonging effect of calorie restriction is due to a decrease in IGF-1 levels. A search for pharmacological modulators of life-span-extending mutations in the GH/IGF-1/insulin signaling pathway and mimetics of caloric restriction is a priority direction in the regulation of longevity. Some literature and our own observations suggest that antidiabetic drugs could be promising candidates for both life span extension and prevention of cancer

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