Unknown

Dataset Information

0

The digitonin-permeabilized pancreatic islet model. Effect of myo-inositol 1,4,5-trisphosphate on Ca2+ mobilization.


ABSTRACT: Glucose-induced insulin secretion is thought to be mediated by submicromolar increases in intracellular Ca2+, although the intracellular processes are not well understood. We have used the previously characterized digitonin-permeabilized insulin-secreting pancreatic islet model to study the role of myo-inositol 1,4,5-trisphosphate (IP3), a putative second messenger for mobilization of intracellular Ca2+. Ca2+ efflux from the endoplasmic reticulum was studied with or without vanadate present to inhibit Ca2+ reuptake. IP3 (10 microM), at a free Ca2+ level of 0.06 microM, increased Ca2+ release by 30% and, when vanadate was present, by 50%. Maximal and half-maximal Ca2+ release was observed at 10 microM- and 2.5 microM-IP3, respectively. IP3 provoked a rapid release that was followed by slow reuptake. Reuptake was diminished in the presence of vanadate. Inositol 1,4-bisphosphate, inositol 1-phosphate and other phosphoinositide metabolites did not have any significant effect. Because increases in Ca2+ levels in the submicromolar range have been previously shown to induce insulin release in digitonin-permeabilized islets, our results are consistent with the concept of IP3 serving as a second messenger for insulin secretion.

SUBMITTER: Wolf BA 

PROVIDER: S-EPMC1144928 | biostudies-other | 1985 May

REPOSITORIES: biostudies-other

Similar Datasets

| S-EPMC1151403 | biostudies-other
| S-EPMC3037600 | biostudies-literature
| S-EPMC7116374 | biostudies-literature
| S-EPMC1133688 | biostudies-other
| S-EPMC7659177 | biostudies-literature
| S-EPMC3672942 | biostudies-literature
| S-EPMC2881802 | biostudies-literature
| S-EPMC1147675 | biostudies-other
| S-EPMC6205300 | biostudies-literature
| S-EPMC2740445 | biostudies-literature