DIRECT EVIDENCE FOR A STIMULATORY EFFECT OF HYPERGLYCEMIA PER-SE ON PERIPHERAL GLUCOSE DISPOSAL IN TYPE-II DIABETES
DIRECT EVIDENCE FOR A STIMULATORY EFFECT OF HYPERGLYCEMIA PER-SE ON PERIPHERAL GLUCOSE DISPOSAL IN TYPE-II DIABETES
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DOI：
10.1172/jci112432
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发表时间：
1986-04-01
影响因子：
15.9
通讯作者：
SACCA, L
中科院分区：
文献类型：
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作者：
CAPALDO, B;SANTORO, D;SACCA, L
通过前臂技术，在生长抑素（SRIF）输注（0.7 mg/h）诱导的胰岛素缺乏的条件下，对6名对照组和6名II型糖尿病患者的肌肉组织葡萄糖摄取的高血糖本身的影响进行了定量。在SRIF输注的第一个60分钟期间，将血糖浓度钳制在其基础值，然后升高至约。200 mg/dl通过可变葡萄糖输注。在SRIF输注期间，包括高血糖期，血浆胰岛素水平保持在或低于5 μ U/ml。对照组和糖尿病患者之间在基础状态下前臂葡萄糖代谢无明显差异。在SRIF输注和eutrophin 60分钟后，前臂葡萄糖摄取从2.1 ± 0.5持续下降。0.7 mg.升-1.cntdot. min-1至1.0 ±. 0.6（P < 0.05），从1.7 . ±. 2至0.4 .+-。0.3糖尿病组与对照组比较差异有显著性（P < 0.02）。随后诱导高血糖引起动脉-深静脉血糖差（P < 0.02-0.01）和前臂葡萄糖摄取（P < 0.01-0.005）显著增加。然而，糖尿病组的反应明显大于对照组。前臂葡萄糖摄取的增量面积为276 . ±. 31 mg. cntdot.升-1.cntdot. 90分钟和532 . ±.对照组和糖尿病组分别为81例（P < 0.02）。在基础状态下，前臂释放乳酸和丙氨酸在对照组和糖尿病受试者作为可比率。尽管葡萄糖摄取率升高，但高血糖后未观察到增加。它的结论是：（1）高血糖本身刺激前臂葡萄糖处置在更大程度上在II型糖尿病患者比正常人;和（2）由此产生的增量的葡萄糖处置不加速前臂释放的三碳化合物。这些数据支持这样的假设，即高血糖本身可能对II型糖尿病中的葡萄糖处理缺陷起代偿作用。
The effect of hyperglycemia per se on glucose uptake by muscle tissue was quantitated in six controls and six type II diabetics by the forearm technique, under conditions of insulin deficiency induced by somatostatin (SRIF) infusion (0.7 mg/h). Blood glucose concentration was clamped at its basal value during the first 60 min of SRIF infusion and then raised to .apprx. 200 mg/dl by a variable glucose infusion. Plasma insulin levels remained at or below 5 .mu.U/ml during SRIF infusion, including the hyperglycemic period. No appreciable difference between controls and diabetics was present in the basal state as to forearm glucose metabolism. After 60 min of SRIF infusion and euglycemia, forearm glucose uptake fell consistently from 2.1 .+-. 0.7 mg .cntdot. liter-1 .cntdot. min-1 to 1.0 .+-. 0.6 (P < 0.05) and from 1.7 .+-. 2 to 0.4 .+-. 0.3 (P < 0.02) in the control and diabetic groups, respectively. The subsequent induction of hyperglycemia caused a marked increase in both the arterial-deep venous blood glucose difference (P < 0.02-0.01) and forearm glucose uptake (P < 0.01-0.005). However, the response in the diabetic group was significantly greater than that observed in controls. The incremental area of forearm glucose uptake was 276 .+-. 31 mg .cntdot. liter-1 .cntdot. 90 min and 532 .+-. 81 in the control and diabetic groups, respectively (P < 0.02). In the basal state, the forearm released lactate and alanine both in controls and diabetic subjects as comparable rates. No increment was observed after hyperglycemia, despite the elevated rates of glucose uptake. It is concluded that (1) hyperglycemia per se stimulates forearm glucose disposal to a greater extent in type II diabetics than in normal subjects; and (2) the resulting increment of glucose disposal does not accelerate the forearm release of three carbon compounds. The data support the hypothesis that hyperglycemia per se may play a compensatory role for the defective glucose disposal in type II diabetes.