IMPAIRED GLUCOSE-TOLERANCE AS A DISORDER OF INSULIN ACTION - LONGITUDINAL AND CROSS-SECTIONAL STUDIES IN PIMA-INDIANS
IMPAIRED GLUCOSE-TOLERANCE AS A DISORDER OF INSULIN ACTION - LONGITUDINAL AND CROSS-SECTIONAL STUDIES IN PIMA-INDIANS
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DOI：
10.1056/nejm198805123181901
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发表时间：
1988-05-12
影响因子：
158.5
通讯作者：
BOGARDUS, C
中科院分区：
文献类型：
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作者：
LILLIOJA, S;MOTT, DM;BOGARDUS, C
葡萄糖耐量受损通常预示着非胰岛素依赖型糖尿病的发展。我们研究了24名皮马印第安人在葡萄糖耐量受损之前和之后的胰岛素作用和分泌，以及代表葡萄糖耐量的整个光谱的254名其他受试者，包括明显的非胰岛素依赖型糖尿病受试者。从正常到糖耐量受损的转变与高胰岛素血症期间葡萄糖摄取的降低相关，从0.018 mmol/min降至0.016 mmol/min（从3.3 mg/kg无脂体重降至2.8 mg/kg无脂体重/min）（p < 0.0003）。平均血浆胰岛素浓度在口服葡萄糖耐量试验期间从1200 pmol/L增加到1770 pmol/L（从167 μ U/ml增加到247 μ U/ml）。在151名具有正常葡萄糖耐量的受试者中，在口服葡萄糖耐量试验期间测量的胰岛素浓度与血浆葡萄糖浓度相关（r = 0.48，P ≤ 0.01）。0.0001）。该关系用于预测葡萄糖耐量受损受试者中1550 pmol/L（216 μ U/ml）的胰岛素浓度（实际值，1590 pmol/L [222 μ U/ml]; P不显著），表明这些受试者具有正常的胰岛素分泌。相反，糖尿病患者的血浆胰岛素浓度随着葡萄糖浓度的增加而降低（r =-0.75，P ≤ 0.05）。0.0001），表明胰岛素分泌不足。这种相对胰岛素缺乏首先出现在血浆葡萄糖浓度的群体频率分布中所见的第二（糖尿病）模式的下端。我们的数据表明，在我们的研究人群中，糖耐量受损主要是由于胰岛素作用受损。相比之下，在非胰岛素依赖型糖尿病患者中，胰岛素作用受损和胰岛素分泌失败都存在。
Impaired glucose tolerance often presages the development of non-insulin-dependent diabetes mellitus. We have studied insulin action and secretion in 24 Pima Indians before and after the development of impaired glucose tolerance and in 254 other subjects representing the whole specturm of glucose tolerance, including subjects with overt non-insulin-dependent diabetes. The transition from normal to impaired glucose tolerance was associated with a decrease in glucose uptake during hyperinsulinemia, from 0.018 to 0.016 mmol per minute (from 3.3 to 2.8 mg per kilogram of fat-free body mass per minute) (p < 0.0003). Mean plasma insulin concentrations increased during an oral glucose-tolerance test, from 1200 to 1770 pmol per liter (from 167 to 247 .mu.U per milliliter). In 151 subjects with normal glucose tolerance, the insulin concentration measured during an oral glucose-tolerance test correlated with the plasma glucose concentration (r = 0.48, P .ltoreq. 0.0001). This relation was used to predict an insulin concentration of 1550 pmol per liter (216 .mu.U per milliliter) in subjects with impaired glucose tolerance (actual value, 1590 pmol per liter [222 .mu.U per milliliter]; P not significant), suggesting that these subjects had normal secretion of insulin. In contrast, plasma insulin concentrations in the diabetics decreased as glucose concentrations increased (r = -0.75, P .ltoreq. 0.0001), suggesting deficient secretion of insulin. This relative insulin deficiency first appears at the lower end of the second (diabetic) mode seen in population frequency distributions of plasma glucose concentrations. Our data show that impaired glucose tolerance in our study population is primarily due to impaired insulin action. In patients with non-insulin-dependent diabetes mellitus, by contrast, impaired insulin action and insulin secretory failure are both present.