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Physiol. Genomics 17: 230-244, 2004. First published February 3, 2004; doi:10.1152/physiolgenomics.00203.2003 Free Article
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Received 8 December 2003; accepted in final form 29 January 2004.
Physiological Genomics 17:230-244 (2004)
1094-8341/04 $5.00 © 2004 American Physiological Society

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

Matthias Bauer1,*, Anne C. Hamm1,*, Melanie Bonaus1, Andrea Jacob2, Jens Jaekel3, Hubert Schorle2, Michael J. Pankratz1 and Joerg D. Katzenberger1

1 Institut fuer Genetik, Forschungszentrum Karlsruhe, 76021 Karlsruhe
2 Institut fuer Pathologie, Universitaet Bonn, 53127 Bonn, Germany
3 Institut fuer Angewandte Informatik, Forschungszentrum Karlsruhe, 76021 Karlsruhe, Germany

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.

microarray analysis; nutrient response; caloric restriction; metabolic signaling; aging/longevity




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