Isolated rat islets were maintained in vitro in a simple perifusion system and the rate of insulin secretion was maintained throughout the period of perifusion. Exposure of the perifused islets to alloxan (20 mg. per cent) for a period of five minutes produced complete inhibition of subsequent glucose-induced insulin secretion with retention of basal secretion. Glucose, mannose and 3-0 methyl glucose provided complete or almost complete protection of the perifused islets from the inhibitory effect of alloxan on glucose-induced insulin release. The order of potencies of various hexoses to protect against alloxan toxicity in vitro was glucose (100 ⋝ 3−0 methyl glucose ⋝ mannose > 2-deoxyglucose > galactose > fructose ≫ L-glucose (0). Mannoheptulose diminished but did not abolish the protective effect of glucose against alloxan. The first phase of tolbutamide-induced secretion was retained after exposure to alloxan. This finding indicated that the beta cells were still viable and suggests that a separate receptor or transport site for tolbutamide may exist on the beta cell. The possible mechanisms by which the hexoses protect the beta cells from alloxan are discussed.

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