Lerner R L, Porte D
J Clin Invest. 1972 Jul;51(7):1624-31. doi: 10.1172/JCI106963.
Previous observations in normal subjects have suggested that when 5-g glucose pulses (P) were given in the following sequence: before (P1) and 45 min after beginning a 300 mg/min glucose infusion (P2); during the 20th hr (P3) and 1 hr after the infusion was stopped (P4); the insulin responses were consistent with a simple two-pool model. One pool is a readily available small storage pool which is refilled by a second, larger, more slowly responding pool that controls basal and steady-state insulin output. The identical protocol was employed to evaluate the insulin responses in 13 nonobese diabetic subjects. DIABETICS HAD BASAL INSULIN LEVELS INDISTINGUISHABLE FROM NORMALS (DIABETICS: 10.7+/-4; normals: 10.7+/-5, mean +/-SD, muU/ml), but had significantly elevated basal glucose levels (diabetics: 161+/-27; normals: 88+/-7, mg/100 ml, P < 0.05). The mean early insulin response (3-5 min Delta IRI) after a 5 g glucose pulse (P1) was significantly diminished in diabetics (diabetics 6.4+/-9; normals: 32.5+/-14, muU/ml, P < 0.01) consistent with a defective storage pool output. The glucose disappearance rate, K(G), decreased in parallel with the early insulin response and the slope of the regression line between these two variables was virtually identical with that calculated from 16 normal subjects. Similar to normal subjects, during the short glucose infusion, the acute insulin response to P2 was diminished in diabetics (P < 0.02). In normal subjects after 20 hr of infusion, the rapid insulin responses to P3 are restored to the preinfusion P1 values, and 1 hr after the infusion was stopped, the responses to P4 are increased twofold (P < 0.001). Diabetics, however, demonstrated decreased early responses to P3 (P < 0.001) and no increased response to P4. In contrast to the diminished acute insulin responses to glucose pulses, diabetics have steady-state insulin levels after 20 hr of glucose infusion similar to those of normal subjects (diabetics: 25.7+/-13; normals: 32.5+/-14, muU/ml). Thus both basal and steady-state insulin levels of diabetics were comparable with those of normal subjects, which suggest that although the rapid insulin response from the storage pool output is defective in diabetics, the more slowly responding pool is intact.
先前对正常受试者的观察表明，当按照以下顺序给予5克葡萄糖脉冲（P）时：在开始以300毫克/分钟的速度输注葡萄糖之前（P1）和之后45分钟（P2）；在输注的第20小时期间（P3）和停止输注后1小时（P4）；胰岛素反应符合简单的双池模型。一个池是一个易于利用的小储存池，它由第二个更大、反应更慢的池重新填充，该池控制基础和稳态胰岛素输出。采用相同的方案评估了13名非肥胖糖尿病受试者的胰岛素反应。糖尿病患者的基础胰岛素水平与正常人无显著差异（糖尿病患者：10.7±4；正常人：10.7±5，平均值±标准差，微单位/毫升），但基础血糖水平显著升高（糖尿病患者：161±27；正常人：88±7，毫克/100毫升，P<0.05）。糖尿病患者在给予5克葡萄糖脉冲（P1）后的平均早期胰岛素反应（3 - 5分钟ΔIRI）显著降低（糖尿病患者6.4±9；正常人：32.5±14，微单位/毫升，P<0.01），这与储存池输出缺陷一致。葡萄糖消失率K（G）与早期胰岛素反应平行下降，这两个变量之间回归线的斜率与从16名正常受试者计算得出的斜率几乎相同。与正常受试者相似，在短时间葡萄糖输注期间，糖尿病患者对P2的急性胰岛素反应降低（P<0.02）。在正常受试者输注20小时后，对P3的快速胰岛素反应恢复到输注前P1值，停止输注1小时后，对P4的反应增加两倍（P<0.001）。然而，糖尿病患者对P3的早期反应降低（P<0.001），对P4无反应增加。与对葡萄糖脉冲的急性胰岛素反应降低相反，糖尿病患者在葡萄糖输注20小时后的稳态胰岛素水平与正常受试者相似（糖尿病患者：25.7±13；正常人：32.5±14，微单位/毫升）。因此，糖尿病患者的基础和稳态胰岛素水平与正常受试者相当，这表明尽管糖尿病患者储存池输出的快速胰岛素反应存在缺陷，但反应更慢的池是完整的。
