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Hypoxia and Nitric Oxide Treatment Confer Tolerance to Glucose Starvation in a 5â²-AMP-activated Protein Kinase-dependent Manner
Ist Teil von
The Journal of biological chemistry, 2002-09, Vol.277 (36), p.32791
Ort / Verlag
American Society for Biochemistry and Molecular Biology
Erscheinungsjahr
2002
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
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 5â²-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 5â²-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.
Sprache
Englisch
Identifikatoren
ISSN: 0021-9258
eISSN: 1083-351X
DOI: 10.1074/jbc.M112270200
Titel-ID: cdi_highwire_biochem_277_36_32791
Format
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