In islets removed from untreated streptozotocin-diabetic rats, the somatostatin-containing cells were unresponsive to changes in glucose concentration, while they did respond to raised cyclic AMP levels. By contrast, in vivo insulin treatment restored the glucose sensitivity of the somatostatin secreting cells. In addition, in vivo insulin treatment resulted in a lowering of the high basal somatostatin secretion rate found in islets from untreated diabetic rats. These changes were made without any alteration of islet insulin content or enhancement of the in vitro insulin secretion. These results indicate that there is not a basic defect in the glucoreceptor of the somatostatin cell in diabetes.

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