Immunoassay Of Endogenous Plasma Insulin In Man

centrations observed in diabetic subjects during the glucose tolerance test are not inconsistent with the less extensive data of Bornstein and Lawrence (1) and Baird and Bornstein (39). Very recently Seltzer and Smith (41), employing the rat diaphragm assay of Vallance-Owen and Hurlock (33), have reported insulin concentrations one hour after glucose, in tolbutamide-sensitive adult diabetics, almost in the normal range, but significantly lower values were observed in juvenile diabetics and adult tolbutamide-insensitive diabetics. To resolve the present finding of a higher than normal integrated insulin output in diabetics during the glucose tolerance test with sustained hyperglycemia in these patients, it must be concluded that the tissues of the maturity-onset diabetic do not respond to his insulin as well as the tissues of the nondiabetic subject respond to his insulin. However, from these observations it cannot be concluded that the early diabetic has the same maximal potential insulin output as the nondiabetic, since in the latter the return of blood sugar to normal levels does not allow for the continued stimulus of prolonged hyperglycemia as in the diabetic. The attempt to produce a sustained stimulus to insulin secretion by repeated administration of glucose to a total of 250 g did result in a more marked insulin secretion in nondiabetic subjects. However, the response of diabetics was still greater indicating that their insulin reserve is not depleted during the 100 g glucose tolerance test. The experiments failed, however, to test maximal insulin secretory capacity of the nondiabetic subjects since a sustained hyperglycemia was not achieved in these patients.

Appreciation of the lack of responsiveness of blood sugar, in the face of apparently adequate amounts of insulin secreted by early maturity-onset diabetic subjects, is obviously of importance in the interpretation of the pathogenesis of this type of diabetes. However, the data at hand can only indicate that absolute insulin deficiency per se is not the cause of the hyperglycemia and suggest other possibilities that merit investigation, namely, 1) abnormal tissues with a high threshold for the action of insulin; 2) an abnormal insulin that acts poorly with respect to hormonal activity in vivo but reacts well immunologically in vitro; 3) an abnormally rapid inactivation of hormonally

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