Effect of Somatostatin on Insulin Secretion Induced by lonophore A23187

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Abstract
Cyclic somatostatin, at a concentration which inhibited both phases of glucose-induced insulin release, completely suppressed monophasic insulin secretion elicited by ionophore A23187. The ability of A23187 to initiate insulin secretion is believed to be highly dependent upon the drug's capacity to influence calcium transport. Thus, the present findings suggest that the negative influence of somatostatin on the insulin secretory process may be exerted on some calcium-related event critical to the release mechanism.