부산대학교 도서관

Several reports have shown that subjects with coronary, cerebral, and peripheral artery diseases have elevated insulin responses to oral glucose compared with control subjects with no evidence of vascular diseases. In this study, 129 survivors of cerebral infarction (CI) were subdivided into two groups (cortical artery group and perforating artery group), and glucose, insulin (IRI), free fatty acid (FFA) and glucagon (IRG) responses to 50 g oral glucose were studied to assess the role of abnormal glucose metabolism in the pathogenesis of CI.Patients with CI showed a significant rise in blood glucose levels after oral administration of glucose. In many of the patients the blood glucose values after oral administration of glucose satisfied the criteria for the diagnosis of diabetes mellitus (DM) of the Japan Diabetic Society, and the new diagnostic criteria for DM or impaired glucose tolerance (IGT) of WHO.The patients with CI had abnormally delayed insulin responses after glucose. The mean concentration of IRI at 30 minutes in the perforating artery group was significantly lower than in healthy subjects and the cortical artery group, and the total IRI (sum of plasma IRI levels at 0, 30, 60 and 120 minutes) in the perforating aterty group was low. The plasma IRI in the cortical artery group showed a delayed response and reached a peak at one hour, but the mean concentration at two hours was significantly higher in the cortical artery group than in the healthy group. As a result, the total IRI was higher in the cortical artery group than in the healthy subjects and the perforating artery group.The fasting FFA levels were higher in both groups of CI than in the healthy subjects. The plasma FFA fell rapidly after ingestion of glucose and no significant difference was found in the declining response.Plasma glucagon in healthy subjects fell significantly after the adminstration of glucose, whereas the levels of plasma glucagon did not decrease after glucose ingestion in many patients with CI.The findings suggest that diabetes with decreased insulin secretion accelerates the development of CI in the distribution of the perforating artety area more than in the cortical artery area, and that hyperinsulinism may play a role in the genesis of atherosclerosis of CI in the cortical artery area.