In a 5-12 year follow-up study of 288 subjects with impaired glucose tolerance after a 100-g glucose load, 48 worsened to overt Type 2 (non-insulin-dependent) diabetes with the elevation of fasting blood glucose. The initial level of blood glucose was a major predictor of subsequent worsening to diabetes. In addition, subjects with a lower insulin response to glucose showed a higher incidence of worsening to the disease, irrespective of blood glucose levels. Multivariate analysis indicated that a diminished insulin response and a high maximal body weight index, as well as a high level of fasting and 2-h glucose values at the initial 100-g oral glucose tolerance test were significant independent risk factors for the development of diabetes in Japanese subjects.
Serum insulin responses to 100 g oral glucose, intravenous tolbutamide, and oral glucose plus intravenous glucagon and tolbutamide, were studied in patients who were definitely diabetic but subsequently improved to have normal glucose tolerance following treatment. "Definite diabetes" was diagnosed when the patient had had fasting blood sugar higher than 150 nag/ 100 ml or had clear diabetic retinopathy plus glucose intolerance. This improved group, whether nonobese or obese, had significantly decreased insulin responses during glucose tolerance test and glucose-glucagon-tolbutamide test, but the insulin response to intravenous tolbutamide was not significantly different from the control. In contrast, in the secondary diabetes group, whose glucose intolerance might be attributable to other diseases than diabetes, insulin response to glucose was enhanced, and was normalized when glucose tolerance became normal. The insulin response to glucose of the prediabetes group (i.e. with both parents diabetic) with normal glucose tolerance was intermediate between those of the ]healthy and diabetes groups. It seems that the low insulin response to glucose is a less easily corrigible feature than glucose intolerance and probably constitutes one of the most fundamental abnormalities in primary diabetes.
To explore the role of endogenous glucocorticoid in insulin secretion, the plasma concentrations of insulin in the fasting state and in response to intravenous administration of glucose were determined in adrenalectomized and sham-adrenalectomized rats. Adrenalectomy produced a decrease in the fasting plasma insulin two days after the operation when there was found no change in the blood glucose levels. Likewise, plasma insulin response to glucose was clearly reduced in adrenalectomized rats, although there was no difference among the two groups in increment of the blood glucose after the glucose load. At this moment, a stimulatory action of insulin on glucose metabolism was rather decreased in the adipose tissue from the adrenalectomized rats when compared with that from the control rats. The pancreatic tissue from the adrenalectomized rats secreted much less amount of insulin in response to perifused glucose not only in the early phase but also in the second phase of release pattern. The pancreas from the adrenalectomized rats treated with dexamethasone showed the opposite changes. These findings support the hypothesis that the endogenous glucocorticoid may play a role in maintaining sensitivity of the B cell to insulinogenic stimuli.
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