INSULIN RESISTANCE IN UREMIA
INSULIN RESISTANCE IN UREMIA
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DOI：
10.1172/jci110067
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发表时间：
1981-01-01
影响因子：
15.9
通讯作者：
WAHREN, J
中科院分区：
文献类型：
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作者：
DEFRONZO, RA;ALVESTRAND, A;WAHREN, J
用正常血糖胰岛素钳夹技术检测了17例慢性尿毒症患者和36例对照组的组织对胰岛素的敏感性。.apprx使血浆胰岛素浓度升高。100u.U/ml，通过可变的葡萄糖输注将血糖浓度维持在基础水平。在正常血糖的这些稳定状态下，葡萄糖输注率是对整个身体摄取的葡萄糖量的衡量。在尿毒症受试者中，胰岛素介导的葡萄糖代谢比对照组(3.71±-)降低了47%。0.20比7.38+-0.26 mg/kg.cntdot。最低标准为0.001)。尿毒症受试者基础肝葡萄糖产生(用[~3H]-3-葡萄糖测定)正常(2.17±-)。0.04 mg/kg.cntdo.Min)，并且正常抑制94.+-。注射胰岛素后为2%。用肝静脉插管技术直接测定6例尿毒症患者和6例正常对照组的内脏净血糖平衡。在吸收后状态下，尿毒症患者内脏葡萄糖产生与之相似(1.57±-)。0.03 mg/kg.cntdo.Min)和对照(1.79+-)。0.20 mg/kg.cntdot。Min)。在持续高胰岛素血症90分钟后，内脏葡萄糖平衡恢复为净摄取，与尿毒症患者相似(0.42.+-)。0.11 mg/kg.cntdot。Min)和对照(0.53.+-.0.12 mg/kg.cntdot。Min)。尿毒症组腿部葡萄糖摄取减少了60%(21。+-)。1比52。+-8微克分子/分毫微米。腿部重量为0.005公斤)，这一下降与全身总葡萄糖代谢的下降密切相关。这些结果表明：生理性高胰岛素血症对肝脏葡萄糖生成的抑制不受尿毒症的影响，胰岛素介导的肝脏葡萄糖摄取在尿毒症患者中是正常的，组织对胰岛素不敏感是尿毒症患者胰岛素抵抗的主要原因。
Tissue sensitivity to insulin was examined with the euglycemic insulin clamp technique in 17 chronically uremic and 36 control subjects. The plasma insulin concentration was raised by .apprx. 100 .mu.U/ml and the plasma glucose concentration was maintained at the basal level with a variable glucose infusion. Under these steady-state conditions of euglycemia, the glucose infusion rate is a measure of the amount of glucose taken up by the entire body. In uremic subjects, insulin-mediated glucose metabolism was reduced by 47% compared with controls (3.71 .+-. 0.20 vs. 7.38 .+-. 0.26 mg/kg .cntdot. min; P < 0.001). Basal hepatic glucose production (measured with [3H]-3-glucose) was normal in uremic subjects (2.17 .+-. 0.04 mg/kg .cntdot. min) and suppressed normally by 94 .+-. 2% following insulin administration. In 6 uremic and 6 control subjects, net splanchnic glucose balance was also measured directly by the hepatic venous catheterization technique. In the postabsorptive state, splanchnic glucose production was similar in uremics (1.57 .+-. 0.03 mg/kg .cntdot. min) and controls (1.79 .+-. 0.20 mg/kg .cntdot. min). After 90 min of sustained hyperinsulinemia, splanchnic glucose balance reverted to a net uptake which was similar in uremics (0.42 .+-. 0.11 mg/kg .cntdot. min) and controls (0.53 .+-. 0.12 mg/kg .cntdot. min). Glucose uptake by the leg was reduced by 60% in the uremic group (21 .+-. 1 vs. 52 .+-. 8 .mu.mol/min .cntdot. kg of leg wt; P < 0.005) and this decrease closely paralleled the decrease in total glucose metabolism by the entire body. These results indicate that: suppression of hepatic glucose production by physiologic hyperinsulinemia is not impaired by uremia, insulin-mediated glucose uptake by the liver is normal in uremic subjects and tissue insensitivity to insulin is the primary cause of insulin resistance in uremia.