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J. Biol. Chem., Vol. 262, Issue 8, 3567-3571, Mar, 1987
TJ Biden, B Peter-Riesch, W Schlegel and CB Wollheim
The role of Ca2+ in the generation of inositol phosphates was investigated
using rat pancreatic islets after steady state labeling with
myo-[2-3H]inositol. Depolarizing K+ concentrations (24 mM) evoked early (2
s) increases in inositol 1,4,5-trisphosphate (Ins-1,4,5-P3) and inositol
1,3,4,5-tetrakisphosphate (Ins-1,3,4,5-P4) as measured by high performance
anion-exchange chromatography. The increase in Ins- 1,4,5-P3 was transient
and was followed by a more pronounced rise in Ins-1,3,4-P3. These effects
were dependent on the presence of extracellular Ca2+ but were not secondary
to release of either neurotransmitters or metabolites of arachidonic acid.
K+ also promoted the breakdown of phosphatidylinositol 4,5-bisphosphate
(PtdIns-4,5-P2) and of the other phosphoinositides. Glucose (16.7 mM) was
less marked in its effects but still promoted rapid increases in
Ins-1,3,4,5-P4 (2 s) and Ins-1,4,5-P3 (10 s) and a slower rise in
Ins-1,3,4-P3 (30 s). The levels of all three metabolites rose steadily over
10 min stimulation. These responses to glucose could be largely, although
not entirely, inhibited by depletion of extracellular Ca2+ or by Ca2+
channel blockade with verapamil (20 microM). Carbamylcholine (0.5 mM) was
the most potent stimulus used evoking early rises in Ins-1,4,5-P3 and
Ins-1,3,4,5-P4 (2 s) followed by Ins-1,3,4-P3 (10 s), effects which were
only partially dependent on extracellular Ca2+. The results suggest that a
Ca2+-mediated PtdIns-4,5-P2 hydrolysis accounts for most of the
Ins-1,4,5-P3 generated in response to glucose but not carbamylcholine. In
addition, glucose may exert effects on inositol phosphate metabolism which
are Ca2+ independent.
Ca2+-mediated generation of inositol 1,4,5-triphosphate and inositol 1,3,4,5-tetrakisphosphate in pancreatic islets. Studies with K+, glucose, and carbamylcholine
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