Abraira C, Graham L A, Lawrence A M
Metabolism. 1975 Oct;24(10):1145-55. doi: 10.1016/0026-0495(75)90151-1.
Improved glucose tolerance follows glucose challenges given in rapid succession, the Staub-Traugott effect. The cause for this facilitated glucose disposal is not clear. Augmented insulin release, prior "insulinization" of cells, and suppression of a pituitary factor or free fatty acids (FFA) are previously suggested mechanisms. For information bearing on the role of the pituitary in this phenomenon, study of the Staub effect was undertaken in hypopituitary patients receiving replacement thyroid, cortisone, and sex-steroid therapy and in normal untreated controls. All subjects received three intravenous injections of glucose (0.5 g/kg) at hourly intervals. Plasma glucose, FFA, and insulin were measured. Whereas a definite Staub effect was seen in each control subject, this phenomenon was conspicuously absent in seven hypopituitary patients similarly studied. Patterns of peripheral insulin response were similar for both groups: FFA levels fell more slowly in the hypopituitary subjects. Normal pituitary function appears to be required for the Staub effect. Incremental peripheral insulin levels do not explain the effect. Subnormal suppression of free fatty acids and impaired induction of key glycolytic and glycogenic enzymes are alternative explantations for the absence of the Staub effect in hypopituitary subjects.
连续快速给予葡萄糖挑战后葡萄糖耐量得到改善，即施陶布-特劳戈特效应。这种促进葡萄糖代谢的原因尚不清楚。先前提出的机制包括胰岛素释放增加、细胞预先“胰岛素化”以及垂体因子或游离脂肪酸（FFA）的抑制。为了了解垂体在这一现象中的作用，对接受甲状腺、可的松和性类固醇替代治疗的垂体功能减退患者以及正常未治疗的对照者进行了施陶布效应的研究。所有受试者每小时静脉注射三次葡萄糖（0.5 g/kg）。测量血浆葡萄糖、FFA和胰岛素。虽然每个对照受试者都出现了明确的施陶布效应，但在同样研究的7例垂体功能减退患者中，这一现象明显不存在。两组的外周胰岛素反应模式相似：垂体功能减退受试者的FFA水平下降较慢。施陶布效应似乎需要正常的垂体功能。外周胰岛素水平的增加并不能解释这种效应。游离脂肪酸抑制不足以及关键糖酵解和糖原生成酶诱导受损是垂体功能减退受试者缺乏施陶布效应的替代解释。
