POTENTIATION OF GLUCOSE-STIMULATED INSULIN RELEASE BY TOLAZAMIDE AND PARADOXICAL ABSENCE OF GLUCOSE FACILITATION (STAUB EFFECT) IN NON-INSULIN-DEPENDENT DIABETES
POTENTIATION OF GLUCOSE-STIMULATED INSULIN RELEASE BY TOLAZAMIDE AND PARADOXICAL ABSENCE OF GLUCOSE FACILITATION (STAUB EFFECT) IN NON-INSULIN-DEPENDENT DIABETES
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DOI：
10.1016/0026-0495(86)90157-5
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发表时间：
1986-04-01
影响因子：
9.8
通讯作者：
SONERU, I
中科院分区：
文献类型：
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作者：
REICH, A;ABRAIRA, C;SONERU, I
重复静脉葡萄糖负荷后葡萄糖耐量的加速（Staub-Traugott效应）以前没有在非胰岛素依赖型糖尿病（NIDDM）中进行过测试。6名明显未接受治疗的受试者接受每小时3次IV葡萄糖耐量试验（GTT）。葡萄糖消失率（K）在负荷之间变化非常小，表明抑制的Staub效应。然而，胰岛素水平随着每次负荷而增加。第一次静脉注射葡萄糖后早期胰岛素释放的特征性损失在第三次注射后恢复。在妥拉磺脲治疗4个月后，空腹血糖从180 ± 100 mg/kg下降到180 ± 100 mg/kg。19至134 .+-. 13毫克/分升。尽管葡萄糖刺激的胰岛素释放的显著增强和早期胰岛素释放的进一步改善，K值再次未能逐步上升。这种矛盾甚至发生在三个额外的主题测试后两年的妥拉磺酰胺治疗，这表明妥拉磺酰胺可能不会改善受体后缺陷，阻碍表达的Staub效应。葡萄糖易化效应对NIDDM治疗的适用性可能仅限于预防措施已重建有效组织对内源性胰岛素反应性的受试者。
Acceleration of glucose tolerance after repetitive intravenous glucose loads (Staub-Traugott effect) has not previously been tested in non-insulin-dependent diabetes (NIDDM). Six overt, untreated subjects were administered three hourly IV glucose tolerance tests (GTT). The glucose disappearance rate (K) changed very little between loads, indicating a suppressed Staub effect. However, insulin levels increased with each load. The characteristic loss of early phase insulin release after the first intravenous glucose injection was recovered with the third injection. After four months of tolazamide treatment the fasting plasma glucose fell from 180 .+-. 19 to 134 .+-. 13 mg/dL. Despite dramatic potentiation of glucose-stimulated insulin release and further improvement of early phase insulin release, K values again failed to progressively rise. This paradox occurred even in three additional subjects tested after two years of tolazamide treatment, suggesting that tolazamide may not ameliorate the postreceptor defects that impede the expression of the Staub effect. The applicability of the glucose facilitatory effect to the treatment of NIDDM might be limited to subjects in whom adjunctive measures have reestablished effective tissue responsiveness to endogenous insulin.