抄録
Insulin responses during 100g glucose tolerance tests (GTT) were compared between three groups of patients with varying degrees of glucose intolerance. Patients who had no disease known to be associated with secondary diabetes were classified as patients with idiopathic diabetes mellitus. Those whose present and past fasting blood glucose (FBG) exceeded 140mg/100ml were assigned to Group A, and the rest of the patients to Group B. Group C included patients with liver disease, thyrotoxicosis, or myocardial infarction, or those treated with corticosteroids or who had undergone gastrectomy. Patients in Group A were found to have consistently subnormal insulin responses whether glucose tolerance was normal (i.e. previous abnormality of glucose tolerance), borderline, or diabetic. In contrast, patients in Group C without fasting hyperglycemia had enhanced rather than decreased insulin responses when glucose tolerance was the more impaired. Patients in Group B had insulin responses similar to those either of Group A or of Group C.
The relationship between the sum of six insulin and six blood glucose values during GTT (ΣIRI and ΣBG) was examined. The ΣBG-ΣIRI plot revealed distinctly different distribution zones for Group A and Group C (Zones A and C). In Group A, ΣIRI values were below 300μU/ml irrespective of ΣBG values. In Group C, ΣIRI tended to increase, paralleling the increase in ΣBG values in the range of ΣBG values lower than 1400mg/100ml. In patients whose ΣBG rose above 1400/100ml during corticosteroid treatment, the ΣIRI values decreased and entered into Zone A. After the cessation of corticosteroids in a few of these patients, the ΣIRI values recovered and reentered Zone C, concomitant with an improvement in glucose tolerance. Similar recovery of insulin response from Zone A to Zone C was also observed after the treatment of two obese diabetic patients. Thus, patients with glucose intolerance due to extra-pancreatic causes may secrete insulin at a higher rate than normal so long as the FBG level remains below 120mg/100ml, but a further deterioration in glucose metabolism may lead to a failure of insulin secretory mechanisms.
