The role of endocrine counterregulation for estimating insulin sensitivity from intravenous glucose tolerance tests
The role of endocrine counterregulation for estimating insulin sensitivity from intravenous glucose tolerance tests
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DOI：
10.1210/jc.2006-0019
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发表时间：
2006-06-01
影响因子：
5.8
通讯作者：
Roden, Michael
中科院分区：
文献类型：
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作者：
Brehm, Attila;Thomaseth, Karl;Roden, Michael
内容：在胰岛素修饰的频繁采样静脉葡萄糖耐量试验期间目的：本研究旨在评估胰岛素诱导的血糖下降对胰岛素敏感性（SI）和葡萄糖有效性的最小模型衍生指数的反调节影响。参与者：13名非糖尿病志愿者（7名男性，6名女性，年龄26 +/-1岁，体重指数22.1 +/-0.7 kg/m2）进行了研究。（0.3 g/kg葡萄糖; 0.03 U/kg胰岛素，20 min）和在相同条件下但用可变葡萄糖输注防止血浆葡萄糖浓度降低至低于正常水平（IM-FSIGT-CLAMP）。5名参与者还接受了正常血糖-高胰岛素血症（1 mU（.）kg（-1.）结果：在IM-FSIGT过程中，血浆葡萄糖在60分钟时下降到其最低点50 +/-3 mg/dl，与血浆胰高血糖素、皮质醇、肾上腺素和GH的升高平行（P < 0.05 vs.基础）。葡萄糖输注速率为4.6 +/- 0.5 mg（.）kg（-1.）在IM-FSIGT-CLAMP期间30至180 min之间的min（-1）阻止了血糖下降和低血糖反调节激素反应。在IM-FSIGT期间，SI约低68%（3.40 +/- 0.36 vs. IM-FSIGT-CLAMP：10.71 +/- 1.06 10（-4.）每mu U/ml的葡萄糖有效性在两种方案之间没有差异（0.024 +/- 0.002 vs. 0.021 +/- 0.003 min（-1），P = NS）。与正常葡萄糖高胰岛素钳夹试验相比，IM-FSIGT的SI以相同的单位表示约低66%（P < 0.001），但在正常葡萄糖高胰岛素钳夹试验和IM-FSIGT-CLAMP之间没有差异（P = NS）。结论：IM-FSIGT期间血糖的短暂下降导致SI的估计值较低，这可以用低血糖的激素反应来解释。
Context: During insulin-modified frequently sampled iv glucose tolerance tests (IM-FSIGT), which allow assessment of insulin action, plasma glucose can markedly decrease.Objective: This study aimed to assess the counterregulatory impact of the insulin-induced fall of glucose on minimal model-derived indices of insulin sensitivity (SI) and glucose effectiveness.Participants: Thirteen nondiabetic volunteers (seven males, six females, aged 26 +/- 1 yr, body mass index 22.1 +/- 0.7 kg/m(2)) were studied.Design: All participants were studied in random order during IM-FSIGT (0.3 g/kg glucose; 0.03 U/kg insulin at 20 min) and during identical conditions but with a variable glucose infusion preventing a decrease of plasma glucose concentration below euglycemia (IM-FSIGT-CLAMP). Five participants additionally underwent euglycemic-hyperinsulinemic (1 mU(.)kg(-1.)min(-1)) clamp tests.Results: Plasma glucose declined during IM-FSIGT to its nadir of 50 +/- 3 mg/dl at 60 min in parallel to a rise (P < 0.05 vs. basal) of plasma glucagon, cortisol, epinephrine, and GH. Glucose infusion rates of 4.6 +/- 0.5 mg(.)kg(-1.)min(-1) between 30 and 180 min during IM-FSIGT-CLAMP prevented the decline of plasma glucose and the hypoglycemia counterregulatory hormone response. SI was approximately 68% lower during IM-FSIGT (3.40 +/- 0.36 vs. IM-FSIGT-CLAMP: 10.71 +/- 1.06 10(-4.)min(-1) per mu U/ml, P < 0.0001), whereas glucose effectiveness did not differ between both protocols (0.024 +/- 0.002 vs. 0.021 +/- 0.003 min(-1), P = NS). Compared with the euglycemic hyperinsulinemic clamp test, SI expressed in identical units from IM-FSIGT was approximately 66% (P < 0.001) lower but did not differ between the euglycemic hyperinsulinemic clamp test and the IM-FSIGT-CLAMP (P = NS).Conclusions: The transient fall of plasma glucose during IM-FSIGT results in lower estimates of SI, which can be explained by hormonal response to hypoglycemia.