HOMEOSTASIS MODEL ASSESSMENT - INSULIN RESISTANCE AND BETA-CELL FUNCTION FROM FASTING PLASMA-GLUCOSE AND INSULIN CONCENTRATIONS IN MAN
HOMEOSTASIS MODEL ASSESSMENT - INSULIN RESISTANCE AND BETA-CELL FUNCTION FROM FASTING PLASMA-GLUCOSE AND INSULIN CONCENTRATIONS IN MAN
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DOI：
10.1007/bf00280883
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发表时间：
1985-01-01
期刊：
影响因子：
8.2
通讯作者：
TURNER, RC
中科院分区：
文献类型：
--
作者：
MATTHEWS, DR;HOSKER, JP;TURNER, RC
稳态基础血浆葡萄糖和胰岛素浓度通过它们在反馈回路中的相互作用来确定。计算机求解的模型已被用于预测由不同程度的β-细胞缺乏和胰岛素抵抗。将患者的空腹值与模型的预测进行比较，可以定量评估胰岛素抵抗和β-缺乏的贡献细胞功能对空腹高血糖的影响（稳态模型评估，HOMA）。通过与胰岛素抵抗和β-胰岛素抵抗的独立测量进行比较，确定了估计的准确度和精确度。使用高血容量钳夹和正常血容量钳夹以及静脉内葡萄糖耐量试验检测细胞功能。通过稳态模型评估获得的胰岛素抵抗估计值与通过使用正常血钳夹（Rs = 0.88，p < 0.0001）、空腹胰岛素浓度（Rs = 0.81，p < 0.0001）和高血钳夹（Rs = 0.69，p < 0.01）获得的估计值相关。与胰岛素受体结合的任何方面均无相关性。不足的β的估计-通过稳态模型评估获得的细胞功能与使用高血压钳夹获得的细胞功能相关（Rs = 0.61，p < 0.01），并且与静脉内葡萄糖耐量试验的估计相关（Rs = 0.64，p < 0.05）。来自该模型的估计的低精度（变异系数：胰岛素抗性为31%，β-胰岛素抗性为32%）。细胞缺陷）限制了它的使用，但模型估计值与患者数据的相关性符合基础葡萄糖和胰岛素相互作用在很大程度上由简单的反馈回路决定的假设。
The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees of .beta.-cell deficiency and insulin resistance. Comparison of a patient''s fasting values with the model''s predictions allows a quantitative assessment of the contributions of insulin resistance and deficient .beta.-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and .beta.-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p < 0.0001), the fasting insulin concentration (Rs = 0.81, p < 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p < 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient .beta.-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p < 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p < 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for .beta.-cell deficit) limits its use, but the correlation of the model''s estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.