Modeling Blood Glucose and Insulin Kinetics in Normal, Diabetic and Obese Subjects

Modeling Blood Glucose and Insulin Kinetics in Normal, Diabetic and Obese Subjects
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正常、糖尿病和肥胖受试者的血糖和胰岛素动力学建模

DOI:
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发表时间:
1973
期刊:
影响因子:
7.7
通讯作者:
G. Vercellone
G. Vercellone
中科院分区:
医学1区
文献类型:
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作者:
G. Segre;G. Turco;G. Vercellone

文献摘要

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二室模型(图 1)和数字计算机技术已应用于分析 26 名正常受试者、16 名糖尿病受试者和 8 名肥胖受试者的葡萄糖和胰岛素控制机制。通过向三组中输注葡萄糖(0.5克/分钟,约300分钟)或以0.33克/千克的脉冲静脉注射葡萄糖来干扰系统;测定血浆胰岛素和葡萄糖水平,并通过同时拟合葡萄糖和胰岛素的实验数据以及通过确定静脉注射的C-14-葡萄糖的血液消失曲线收集的附加信息来求解模型。根据表征模型的七个参数,对两组的判别分析显示正常受试者和糖尿病受试者(输注或脉冲葡萄糖)以及正常受试者和肥胖受试者(输注葡萄糖)之间存在统计学上的显着差异。糖尿病患者的显着特征(除了明显的高血糖之外)是 λ21 的降低(图 1),这是衡量胰岛素对葡萄糖负荷反应的参数。肥胖受试者的显着特征是 λ21 增加和 -λ21 减少,该参数测量胰岛素对葡萄糖的反应。这些动态特征与目前对这些病理状态下葡萄糖和胰岛素控制机制受损的认识一致。
A two-compartment model (figure 1) and digital computer technics have been applied to the analysis of glucose and insulin control mechanisms in twenty-six normal, sixteen diabetic, and eight obese subjects. The system was perturbed by infusing glucose (0.5 gm./min. for about 300 minutes) into the three groups or by injecting glucose intravenously as an impulse of 0.33 gm./kg.; plasma insulin and glucose levels were determined and the model was solved by simultaneously fitting to it the experimental data for glucose and insulin, and the additional information gathered by determining the blood disappearance curve of intravenously injected C-14-glucose. A discriminant analysis for two groups gave a statistically significant separation between normal and diabetic subjects (with infused or impulsive glucose) and between normal and obese subjects (with infused glucose) on the grounds of the seven parameters that characterize the model. The prominent feature of the diabetics (in addition to the obvious hyperglycemia) was a decrease of λ21 (figure 1), a parameter which measures the insulin response to a glucose load. The prominent feature of the obese subjects was an increase of λ21 and a decrease of —λ21, a parameter which measures the glucose response to insulin. These dynamic characteristics are in agreement with present knowledge of the impairment of glucose and insulin control mechanisms in these pathologic states.