Potentiation by glucose metabolites of inositol trisphosphate-induced calcium mobilization in permeabilized rat pancreatic islets.
作者： RS Rana , M Ch Sekar , RJ Mertz , LE Hokins , MJ MacDonald
DOI: 10.1016/S0021-9258(19)76465-5
关键词:
摘要: Saponin-permeabilized rat pancreatic islets degraded exogenously added inositol 1,4,5-trisphosphate (IP3), and degradation was inhibited in the presence of either fructose 1,6-bisphosphate or diphosphoglycerate. The addition fructose-1,6-P2 diphosphoglycerate to 45Ca2+-labeled permeabilized potentiated 45Ca2+ release caused by IP3 (by generated endogenously carbachol guanosine 5'-3-O-(thio)triphosphate (GTP gamma S). effect on correlated well with effects these agents recovery radioactivity IP3. These results further support our previous proposal that intracellular calcium mobilization may be sustained part via inhibition metabolites produced during stimulation insulinotropic concentrations glucose (Rana, R.S., Sekar, M.C., Hokin, L.E., MacDonald, M.J. (1986) J. Biol. Chem. 261, 5237-5240).
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