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.

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

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

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 Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1

2018 ◽  
Vol 74 (2) ◽  
pp. 155-162 ◽  
Author(s):  
Alberto Diaz-Ruiz ◽  
Andrea Di Francesco ◽  
Bethany A Carboneau ◽  
Sophia R Levan ◽  
Kevin J Pearson ◽  
...  
Keyword(s):  
Caloric Restriction ◽  
Aging Process ◽  
Laboratory Animals ◽  
Metabolic Flexibility ◽  
Life Span Extension ◽  
Tumor Susceptibility ◽  
Beneficial Effects ◽  
Energy Sensor ◽  
Nonpharmacological Intervention

Abstract Caloric restriction (CR) is the most potent nonpharmacological intervention known to both protect against carcinogenesis and delay aging in laboratory animals. There is a growing number of anticarcinogens and CR mimetics that activate NAD(P)H:quinone oxidoreductase 1 (NQO1). We have previously shown that NQO1, an antioxidant enzyme that acts as an energy sensor through modulation of intracellular redox and metabolic state, is upregulated by CR. Here, we used NQO1-knockout (KO) mice to investigate the role of NQO1 in both the aging process and tumor susceptibility, specifically in the context of CR. We found that NQO1 is not essential for the beneficial effects of CR on glucose homeostasis, physical performance, metabolic flexibility, life-span extension, and (unlike our previously observation with Nrf2) chemical-induced tumorigenesis.

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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