Plasma levels of insulin were determined during standard oral glucose tolerance tests and during cortisone glucose tolerance tests performed upon “nondiabetic” subjects (normal standard GTT) who were first degree relatives of diabetic patients. The standard test was also performed upon mildly diabetic patients and healthy control subjects. The results of the standard glucose tolerance test (levels of plasma insulin and blood glucose) did not differentiate the relatives with positive cortisone glucose tolerance tests (subclinical diabetes) from those with negative cortisone glucose tolerance tests although in both groups levels of plasma insulin were lower than in healthy subjects. However, the results of the cortisone glucose tolerance test did distinguish the group with subclinical diabetes from the relatives with negative tests since the secretion of insulin was delayed and insufficient in the subjects with positive testsl During the standard test patients with mild “maturityonset” diabetes showed delayed and insufficient secretion of insulin as compared to the healthy subjects.

It is concluded that during the cortisone glucose tolerance test, “nondiabetic” relatives of diabetic patients who have positive tests (subclinical diabetes) exhibit a defect in the secretion of insulin which distinguishes them from subjects with negative tests. This defect is similar in pattern to that observed in mildly diabetic patients during the standard test. This deficiency in the secretion of insulin represents an important part of the mechanism which induces a positive cortisone glucose tolerance test.

This demonstration that, in some relatives of diabetics, a grossly normal standard glucose tolerance can exist at a time when decreased reserve insulin secretory capacity can be measured, justifies a careful evaluation of whether some form of therapy is indicated at this stage of the disease (subclinical diabetes) and, if so, what form it should be. The meaning of the statistically significant subnormal response of plasma insulin to a standard glucose load in relatives with negative cortisone glucose tests is not yet apparent. Since in them the reserve insulin secretory capacity, as measured by the CGTT, remains intact, it is premature, pending additional data, to raise the question of possible treatment of this group.

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