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J. Biol. Chem., Vol. 277, Issue 36, 32791-32798, September 6, 2002
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From the Hypoxia is a critical event for higher organisms,
and cells and tissues react by increasing the oxygen supply by
vasodilatation, angiogenesis, and erythropoiesis and maintaining
cellular energy by increasing glycolysis and inhibiting anabolic
pathways. Stimulation of glycolysis has been regarded as the main
response that increases energy production during hypoxia; however,
there is an obvious conflict during ischemia, because both the oxygen
and glucose supply are insufficient. In this study, we found that
exposure of HepG2 cells and normal fibroblasts to hypoxia induces
cellular tolerance to glucose starvation. The tolerance induced by
hypoxia is dependent on several amino acids, indicating a switch from glucose to amino acids as the energy source. When antisense RNA expression vector for 5'-AMP-activated protein kinase or protein kinase
B/Akt was transfected into HepG2 cells, the induction of tolerance to
glucose was greatly inhibited, indicating that the tolerance was
dependent on 5'-AMP-activated protein kinase and protein kinase B/Akt.
Similar tolerance was induced by nitric oxide exposure. The tolerance
induced was observed in various cells and may represent a previously
unknown physiological response related to hypoxia-preconditioning and
tumor progression:austerity.
Hypoxia and Nitric Oxide Treatment Confer Tolerance to Glucose
Starvation in a 5'-AMP-activated Protein Kinase-dependent
Manner*
§,,,,,, and Investigative Treatment Division, National
Cancer Center Research Institute East 6-5-1, Kashiwanoha, Kashiwa,
Chiba 277-8577 and the ¶ Department of Biochemistry, Nagoya
University School of Medicine Tsurumai-chou, Showa-ku,
Nagoya 466-8550, Japan
*
This work was supported in part by a grant for the Second
Term Comprehensive Strategy for Cancer Control from the Ministry of
Health and Welfare and a grant-in-aid for Cancer Research from the
Ministry of Education, Science, Sports, and Culture, Japan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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