Insulin Secretion in Type II Diabetics: In Vivo and in Vitro Investigation1)

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Abstract
Many cases of type II diabetes present an anomaly of insulin secretion which is characterized by a missing, reduced, or delayed glucose-stimulated insulin output from the beta cell. We aimed at finding out whether this characteristic disorder is a consequence of reduced beta cell mass or of a more functional disturbance. In the latter case it was to be clarified whether the disturbed beta cell “glucoreceptor” function represents a qualitative or rather a quantitative difference. By the evaluation of insulin secretion and of carbohydrate tolerance during oral and/or intravenous intake of glucose, and after intravenous application of tolbutamide or glucagon the defective insulin secretion in type II diabetics was found to represent a more functional disturbance which could not be explained by reduction of beta cell mass. Thus it was concluded that the anomaly of insulin secretion mentioned above might be a consequence of a qualitative defect of the glucoreceptor. To prove this, isolated human islets (insulin secretion under incubation with glucose, measurements of 3H-leucine incorporation and of the insulin content) were also studied. In contrast to the in vivo results, insulin release of the isolated islets of type II diabetics was normal. From this it must be concluded that the glucoreceptor of the beta cell, which in vivo reacts in a qualitatively different manner from that of subjects with intact metabolism, is not irreversibly disturbed. These discrepancies between the in vivo and in vitro results could possibly be explained by the existence of circulating or of intrapancreatic antagonists of glucose action on insulin secretion or by an increased responsiveness of the islets of diabetics to normal concentrations of inhibiting substances.

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