Defective Ca++ handling and insulin release in islets of diabetic hamsters and mice.

In islets from normal Chinese hamsters preloaded with 45Ca, glucose-induced biphasic insulin release was accompanied by increased 45Ca++ efflux. Islets from diabetic hamsters showed decreased insulin release and no rise in 45Ca++ efflux. No rise in 45Ca++ efflux was seen, even when insulin release was potentiated by 3-isobutyl-1-methylxanthine (IBMX). Since glucose-induced 45Ca++ uptake was normal in diabetic hamsters a defect in cellular Ca++ handling may be involved in the defective insulin release. A similar decrease of glucose-induced insulin release in islets from diabetic C57BL/KsJ-db/db mice was, on the other hand, associated with a small increase in 45Ca++ efflux. In these islets, IBMX potentiated both insulin release and 45Ca++ efflux suggesting that the release defect may be restricted to glucose.