Stress-induced glucose uptake in bovine chromaffin cells: a comparison of the effect of arsenite and anisomycin.
The effect of the toxic chemical Na-arsenite and the protein synthesis inhibitor anisomycin on glucose transport in primary cultures of bovine chromaffin cells was compared using the effect of insulin-like growth factor I (IGF-I) as a reference. The enhanced uptake of glucose obtained in response to arsenite and anisomycin reached maximum after 60 min, with the response to anisomycin being delayed in onset relative to that of arsenite. At maximal doses the arsenite effect was consistently higher than that of anisomycin and comparable to the approximately 2-fold effect produced by IGF-I. The selective inhibitor of stress-activated protein kinase 2 (SAPK2), SB 203580, inhibited completely anisomycin-induced glucose uptake but only partly suppressed uptake stimulated by arsenite. Both substances, in concentrations producing maximal effects on glucose transport, led to a strong phosphorylation of SAPK2. In contrast to the effect on glucose transport, the arsenite-induced phosphorylation of SAPK2 was relatively slow compared to the anisomycin-induced activation. The results indicate that glucose uptake induced by the two types of cellular stress are mediated by at least two different signaling pathways, which also differ from that activated by IGF-I.
Fladeby
C
C
Department of Physiology, University of Bergen, Arstadveien 19, 5009, Bergen, Norway. catherine.fladeby@pki.uib.no
Serck-Hanssen
G
G
D000818:Animals; D000841:Anisomycin / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D018053:Arsenites / Q000494:pharmacology*; D001692:Biological Transport / Q000187:drug effects; D002417:Cattle; D019439:Chromaffin Cells / Q000187:drug effects* / Q000378:metabolism; D003847:Deoxyglucose / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D020536:Enzyme Activators / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D007375:Interleukin-1 / Q000494:pharmacology; D048031:JNK Mitogen-Activated Protein Kinases; D020929:Mitogen-Activated Protein Kinase Kinases / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000494:pharmacology; D009997:Osmotic Pressure; D010766:Phosphorylation; D015398:Signal Transduction; D017670:Sodium Compounds / Q000494:pharmacology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D015854:Up-Regulation; D048051:p38 Mitogen-Activated Protein Kinases
D018053:Arsenites; D020536:Enzyme Activators; D004791:Enzyme Inhibitors; D007375:Interleukin-1; D017670:Sodium Compounds; D014409:Tumor Necrosis Factor-alpha; C017947:sodium arsenite; D000841:Anisomycin; D003847:Deoxyglucose; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D020929:Mitogen-Activated Protein Kinase Kinases; D005947:Glucose