Lack of Influence of Insulin-induced Hypoglycemia on Alimentary Hyperglycemia

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Abstract
Studies were designed to determine the effect, in diabetic patients, of insulin induced hypoglycemia upon alimentary hyperglycemia. The following results were obtained. In a 4-hr. study, as a control day, each of 4 patients was given his usual insulin 1 hr. before the oral administration of 100 g of glucose. On another occasion, under identical conditions, hypoglycemia was produced during the hour preceding glucose administration, by intravenous administration of Crystalline Insulin. There was no greater impairment of glucose tolerance during the subsequent 3 hr. than noted in the control study. In 10 patients, maintained on constant diets for 3 consecutive days, blood sugars were determined at frequent intervals from 7 a.m. to 10 p.m. each day. Each patient, if insulin dependent, received his usual dose before breakfast on all 3 days. On the 2nd day the adminis -tration of additional subcutaneous Crystalline Insulin produced hypoglycemia during the forenoon. No carbohydrate supplementation was given and generally the hypoglycemia was corrected only by lunch given at the usual time. The postprandial blood sugar elevations for the balance of that day and throughout the 3rd day were no greater than those of the 1st or control day. In 1 patient 6 identical studies were performed. In each instance 25 g of glucose was given by mouth at 7 a.m. on each of 3 consecutive days. Blood sugars were measured at 2-hr. intervals from 8 a.m. to 12 noon. On day 2 hypoglycemia was produced by the administration of 15-25 U. Crystalline Insulin after the 8 a.m. blood specimen was drawn. Although mean blood sugars were statistically significantly higher on day 3 than on day 1 at 8 a. m. and 12 noon, the quantitative measurement of urine sugar showed no increase over that of the control day on either the day of hypoglycemia or the folllowing day. These data do not support the concept, in patients with diabetes mellitus, that hypoglycemia is followed by further impairment of glucose tolerance.

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