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.
Effect of Alloxan on Insulin Secretion in Isolated Rat Islets Perifused in Vitro
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Tatsuo Tomita, Paul E Lacy, Franz M Matschinsky, Michael L McDaniel; Effect of Alloxan on Insulin Secretion in Isolated Rat Islets Perifused in Vitro. Diabetes 1 June 1974; 23 (6): 517–524. https://doi.org/10.2337/diab.23.6.517
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