Cobalt (Co'++) inhibited glucose-, leucine-, and K'+-induced immunoreactive insulin (IRI)release by isolated rat islets. This inhibition of the insulinotropic effect of glucose was dose dependent, affected both phases of secretion, was very rapid, and was well reversible. It exhibited a kinetics similiar to that of Ca'++ omission, and the metal (2.5 mM) prevented Ca'++ reintroduction from restoring a normal rate of IRI release. Theophylline (2 mM) partially overcame the inhibitory effect of 0.5 mM Co'++, but not that of 2.5 mM. Glucose-induced secretion was lessmarkedly reduced by 0.5 mM Co'++ in the absence of Mg'++ or in the presence of 7.5 mM Ca'++. Even at 12.5 mM, the metal did not alter glucose oxidation by theislets. By contrast, Ca uptake by islet cells was reversibly diminished (55%) in the presence of 1.25 mM Co'++. Calcium influx (measured after 2.5 min) was aslo reduced by Co'++ to a degree that did not change after longer incubation periods. It is concluded that Co'++ inhibits IRI release mainly through an antaognistic action on Ca entry in beta cells.
The role of HCO3 ions in pancreatic beta-cell functions was evaluated with isolated rat islets. The early phase of insulin release was absent when HCO3 ions were omitted from the medium prior to glucose stimuation, but was augmented if HCO3- withdrawal or reintroduction coincided with glucose increase. The inhibition of the late phase augmented as a function of the duration of HCO3- absence, and its reversibility upon readmission of the anion was delayed. Theophylline and cytochalasin B partially corrected the inhibition of the late phase but failed to restore a rapid response. In the presence of 5 mM NaHCO3, the early response was delayed but the total response was normal. In a HCO3--free medium, glucose oxidation and utilization and glucose transport in islet cells were unaltered. Uptake of calcium was reduced in the absence of HCO3 ions, but normal in 5 mM HCO3-. The results document the importance of HCO3- in insulin release and show that the two phases of glucose-induced secretion are differentially modified by its omission. Some of these findings may be explained by alterations in Ca++ uptake by islet cells. It is suggested that the mechanisms regulating insulin granule extrusion upon stimulation by glucose may be partially different for the two phases of release.
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