抄録
Plasma concentrations of apolipoproteins (apo) A-I, A-II, B, C-II and E were measured in the 79 noninsulin-dependent (type II) diabetics. The diabetics consisted of 24 patients on dietary treatment alone (diet group), 16 patients treated with oral hypoglycemic agents (mostly glibenclamide: oral drug group), 15 patients treated with insulin (insulin group) and 24 untreated patients (pretreatment group). The data were analyzed after subdividing each group into the following two subgroup on the basis of fasting blood glucose levels and HbA1 levels: (1) the patients in good control and (2) the patients in poor control. Mean (±SE) ages were 61.2±2.4, 59.5±2.6, 61.5±2.7, 67.3±0.3, 67.6±3.7, 58.3±3.2, 59.3±1.7 in diet-good control group, diet-poor control group, oral druggood control group, oral drug-poor control group, insulin-good control group, insulin-poor control group and pretreatment group, respectively. Fasting blood glucose levels and HbA1 levels in parenthesis were 105.2±2.9mg/100ml (7.4±0.3%), 151.5±11.3 (9.6±0.2), 97.5±6.2 (8.3±0.4), 162.0±13.0 (11.0±0.2), 107.7±8.3 (8.4±0.5), 198.3±16.8 (11.3±0.4) and 175.9±12.4 (10.8±0.5) in the groups in the same order as above, respectively. HDL was fractionated by the method of heparin-MnCl2 precipitation. Plasma apo A-I, A-II, B, C-II and E were measured by single radial immunodiffusion using the commercially available plate (Daiichi Chemical Pharmaceutical Co., Tokyo). Both plasma cholesterol and triglyceride were significantly higher in the diabetic groups than control. HDL-cholesterol was significantly lower in diet-good control group than control. Plasma apo B concentrations were significantly increased in the diabetics (diet-poor control group: 130.0±21.6mg/100ml, oral drug-good control group: 108.9±21.1, insulin-poor control group: 130.5±23.5, pretreatment group: 122.3±23.5vs. control group: 87.9±20.5). Plasma apo C-II concentrations were significantly higher in the diabetics (diet-poor control group: 5.5±2.9mg/100ml, insulin-poor control group: 6.7±1.9, pretreatment group: 5.0±2.2vs. control group: 2.4±0.8). Plasma apo E concentrations were significantly higher in the diabetics (diet-poor control group: 5.3±2.1mg/ml, insulin-poor control group: 5.9±1.8, pretreatment group: 4.4±1.3vs. control group: 3.4±0.8). Plasma apo A-I concentrations in diabetics were not significantly different from those of control. Plasma apo A-II concentration was significantly lower in diet-good control group (25.6±5.3mg/100ml) than control (29.5±3.4). The effects of diabetic control on plasma apolipoproteins level were investigated. In diet group, plasma concentrations of apo B and apo E were significantly higher in the diabetics with poor control than those with good control (p<0.005 in apo B and p<0.05 in apo E). In insulin group, plasma concentrations of apo C-II and apo E were significantly higher in poor control subgroup as compared to good control subgroup (p<0.005 in apo C-II and p<0.05 in apo E). In addition, apolipoprotein levels were measured before and after treatment in 4 diabetics. Plasma concentrations of apo B, C-II and E showed a tendency to decrease with diabetic control. The present study suggested that plasma apolipoprotein concentrations could be one of the indices of metabolic derangement in the noninsulindependent diabetics.
