Somatostatin Inhibition of Glucose-, Tolbutamide-, Theophylline-, Cytochalasin B-, and Calcium-Stimulated Insulin Release in Monolayer Cultures of Rat Endocrine Pancreas
Somatostatin inhibited insulin secretion stimulated by glucose, tolbutamide, glucose-theophylline, glucose-cytochalasin B and Ca in monolayer cell cultures of neonatal rat endocrine pancreas. Both 2-deoxyglucose-inhibited glucose-induced insulin release and basal insulin secretion occurring at glucose 1.7 mM were further reduced by somatostatin. In the presence of somatostatin, 1.0 .mu.g/ml, insulin secretion due to glucose, tolbutamide, or glucose-cytochalasin B were inhibited to levels below the basal secretion seen with glucose 1.7 mM. Insulin secretion stimulated by Ca, and especially by glucose plus theophylline, remained considerably above basal insulin levels, even with somatostatin 1.0 .mu.g/ml. For all stimuli except Ca, at lower concentrations of somatostatin (0.001-0.10 .mu.g/ml) but not at somatostatin 1.0 .mu.g/ml, increased stimulus concentration partially reversed inhibition by somatostatin. For Ca, even at somatostatin 1.0 .mu.g/ml, insulin release was greater when the Ca concentration was raised. Since net Ca uptake by the .beta. cell or intracellular translocation of Ca within the .beta. cell from an organelle-bound pool to a cytoplasmic pool may trigger insulin secretion through interaction of Ca with the microtubular-microfilamentous system, the inhibition by somatostatin of Ca influx might explain the findings.