Journal of the Japan Diabetes Society
Online ISSN : 1881-588X
Print ISSN : 0021-437X
ISSN-L : 0021-437X
Impaired IRG Response to Insulin-Induced Hypoglycemia in Diabetes
Hiroyuki ToyoshimaTakashi YoshidaKyohei NonakaSeiichiro Tarui
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1978 Volume 21 Issue 3 Pages 191-202

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Abstract
Intravenous insulin tolerance tests (ITT) were performed on 16 normal and 35 diabetic subjects. The purpose of the study was to test the plasma IRG response to insulin-induced hypoglycemia in diabetics, and to determine whether any relationship exists between the IRG responses on ITT and IRI responses on O-GTT in diabetics. In normal subjects, the blood sugar level declined from a basal level of 86±3 (mean±SEM) mg/dl to a minimum of 33±2 mg/dl at 20 min after the injection of MC-Actrapid insulin (0.1 unit/kg body weight). In diabetics, it declined from a basal level of 142±10 mg/dl to a minimum of 42±5 mg/dl at 45 min. after the insulin injection (0.2-0.3 unit/kg body weight). Hypoglycemic symptoms were recognized in all subjects, including normals and diabetics. The plasma IRG level of normals rose from a base-line value of 64±11pg/ml to a peak of 262±45 pg/ml at 30 min. after stimulation, whereas that in diabetics rose from 43±4 pg/ml to 137±21 pg/ml. The IRG responses in diabetics were thus significantly reduced (p<0.01) compared to those in normals. There was a significant negative correlation between fasting blood sugar level and IRG response to ITT in diabetic subjects (p<0.025). In 24 diabetics, a significant positive correlation was found between the IRI response in O-GTT and the IRG response in ITT (p<0.05). This suggests a parallelism in the degree of impairment of both pancreatic A and B cells in diabetics. In arginine tolerance tests (ATT), the plasma IRG response in diabetics was more marked than that in normals. Thus, in diabetics, both an IRG hyporesponse to ITT and a hyperresponse to ATT coexist. This discrepancy may be best explained by assuming some involvement of extrapancreatic IRG in ATT. On the other hand, only pancreatic glucagon responds to ITT. The IRG response to ITT may thus be considered as more specific for pancreatic A cell function than the IRG response to ATT.
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