Mäkimattila S, Virkamäki A, Malmström R, Utriainen T, Yki-Jarvinen H
Department of Medicine, University of Helsinki Central Hospital, Finland.
J Clin Endocrinol Metab. 1996 Feb;81(2):707-12. doi: 10.1210/jcem.81.2.8636292.
We determined whether insulin resistance in Type I diabetes is caused by a defect in glucose extraction or blood flow and whether it is the rate of glucose metabolism rather than insulin that increases blood flow in these patients. To make this determination, 9 Type I diabetic patients (age 33 +/- 3 yr, body mass index 24 +/- 1 kg/m2, HbA1c 8.3 +/- 0.1%) and 10 matched normal subjects were first studied under normoglycemic hyperinsulinemic conditions. The diabetic patients were then restudied under similar conditions, but now whole body glucose uptake was normalized by glucose mass-action (glucose 8.7 +/- 0.6 mmol/L). During normoglycemia, rates of whole body (46 +/- 2 vs. 66 +/- 3 mumol/kg.min, P < 0.001) and forearm (47 +/- 9 vs. 78 +/- 7 mumol/kg forearm.min, P < 0.05) glucose uptake were decreased in the diabetic patients, because of a 32% decrease in the glucose AV-difference (1.5 +/- 0.2 vs. 2.2 +/- 0.2 mmol/L, P < 0.05). Forearm blood flow was similar in the diabetic patients (3.6 +/- 0.7 mL/dl.min) and normal subjects (3.7 +/- 0.3 mL/dL.min). During matched rates of whole body glucose uptake (68 +/- 1 vs. 66 +/- 3 mumol/kg.min, normoglycemic study in controls vs. hyperglycemic study in the diabetic patients), the glucose AV-difference across the forearm was 64% higher than during normoglycemia (2.4 +/- 0.3 vs. 1.5 +/- 0.2 mmol/L, P < 0.05). Forearm blood flow (3.6 +/- 0.4 mL/dL.min) under conditions of matched glucose flux was similar to that during the normoglycemic study. We conclude that a defect in glucose extraction rather than blood flow characterizes insulin resistance in uncomplicated Type I diabetes. The signal for the flow increase is insulin and not the rate of glucose metabolism.
我们确定了I型糖尿病中的胰岛素抵抗是否由葡萄糖摄取或血流缺陷引起，以及在这些患者中增加血流的是葡萄糖代谢速率而非胰岛素。为了做出这一判断，首先在血糖正常高胰岛素血症条件下对9名I型糖尿病患者（年龄33±3岁，体重指数24±1kg/m²，糖化血红蛋白8.3±0.1%）和10名匹配的正常受试者进行了研究。然后在类似条件下对糖尿病患者进行再次研究，但此时通过葡萄糖质量作用使全身葡萄糖摄取正常化（葡萄糖8.7±0.6mmol/L）。在血糖正常期间，糖尿病患者的全身（46±2对66±3μmol/kg·min，P<0.001）和前臂（47±9对78±7μmol/kg前臂·min，P<0.05）葡萄糖摄取率降低，原因是葡萄糖动静脉差值降低了32%（1.5±0.2对2.2±0.2mmol/L，P<0.05）。糖尿病患者的前臂血流（3.6±0.7mL/dl·min）与正常受试者（3.7±0.3mL/dL·min）相似。在全身葡萄糖摄取率匹配时（68±1对66±3μmol/kg·min，对照组血糖正常研究对糖尿病患者高血糖研究），前臂的葡萄糖动静脉差值比血糖正常时高64%（2.4±0.3对1.5±0.2mmol/L，P<0.05）。在葡萄糖通量匹配的条件下，前臂血流（3.6±0.4mL/dL·min）与血糖正常研究期间相似。我们得出结论，单纯性I型糖尿病中的胰岛素抵抗特征是葡萄糖摄取缺陷而非血流缺陷。血流增加的信号是胰岛素而非葡萄糖代谢速率。
