Capaldo B, Santoro D, Riccardi G, Perrotti N, Saccà L
J Clin Invest. 1986 Apr;77(4):1285-90. doi: 10.1172/JCI112432.
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 approximately 200 mg/dl by a variable glucose infusion. Plasma insulin levels remained at or below 5 microU/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 X liter-1 X min-1 to 1.0 +/- 0.6 (P less than 0.05) and from 1.7 +/- .2 to 0.4 +/- 0.3 (P less than 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 less than 0.02-0.01) and forearm glucose uptake (P less than 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 X liter-1 X 90 min and 532 +/- 81 in the control and diabetic groups, respectively (P less than 0.02). In the basal state, the forearm released lactate and alanine both in controls and diabetic subjects at 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.
通过前臂技术，在六名对照者和六名II型糖尿病患者中，对生长抑素（SRIF）输注（0.7毫克/小时）诱导的胰岛素缺乏情况下，高血糖本身对肌肉组织葡萄糖摄取的影响进行了定量研究。在SRIF输注的前60分钟，血糖浓度被钳制在其基础值，然后通过可变葡萄糖输注将其提高到约200毫克/分升。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微单位/毫升。在基础状态下，对照者和糖尿病患者在前臂葡萄糖代谢方面没有明显差异。在SRIF输注60分钟和血糖正常后，对照者和糖尿病患者组的前臂葡萄糖摄取分别从2.1±0.7毫克·升⁻¹·分钟⁻¹持续下降至1.0±0.6（P<0.05）和从1.7±0.2下降至0.4±0.3（P<0.02）。随后诱导的高血糖导致动脉-深静脉血糖差值（P<0.02 - 0.01）和前臂葡萄糖摄取（P<0.01 - 0.005）均显著增加。然而，糖尿病组的反应明显大于对照组。对照者和糖尿病患者组前臂葡萄糖摄取的增量面积分别为276±31毫克·升⁻¹·90分钟和532±81（P<0.02）。在基础状态下，对照者和糖尿病患者的前臂以相当的速率释放乳酸和丙氨酸。尽管葡萄糖摄取率升高，但高血糖后未观察到增加。结论是：（1）高血糖本身在II型糖尿病患者中比在正常受试者中更大程度地刺激前臂葡萄糖处置；（2）由此产生的葡萄糖处置增加并未加速前臂三碳化合物的释放。这些数据支持了高血糖本身可能对II型糖尿病中葡萄糖处置缺陷起补偿作用的假设。
