Lee K U, Kim S Y, Lee H K, Min H K
Diabetes Res Clin Pract. 1985 Dec;1(4):211-20. doi: 10.1016/s0168-8227(85)80014-0.
To evaluate the role of insulin receptors in the pathogenesis of insulin resistance observed in glucocorticoid excess, we measured 125I-insulin binding to circulating erythrocytes in 7 patients with Cushing's syndrome and 7 patients with adrenal insufficiency. Insulin receptor binding was higher in Cushing's syndrome and was lower in adrenal insufficiency, compared to normal subjects. Insulin binding decreased after transsphenoidal surgery in 2 patients with Cushing's syndrome. In addition, glucocorticoid treatment in 6 patients with adrenal insufficiency resulted in the increase of insulin binding. The biological significance of this phenomenon must await further investigation, but it does suggest that insulin resistance in glucocorticoid excess should be interpreted as an alteration of cellular mechanisms of insulin at a step distal to the insulin receptor. Increased insulin binding to the receptor is probably modulated by postreceptor events.
为评估胰岛素受体在糖皮质激素过多所致胰岛素抵抗发病机制中的作用，我们检测了7例库欣综合征患者和7例肾上腺功能不全患者循环红细胞对¹²⁵I胰岛素的结合情况。与正常受试者相比，库欣综合征患者的胰岛素受体结合率较高，而肾上腺功能不全患者的则较低。2例库欣综合征患者经蝶窦手术后胰岛素结合率降低。此外，6例肾上腺功能不全患者接受糖皮质激素治疗后胰岛素结合率升高。这一现象的生物学意义有待进一步研究，但它确实提示糖皮质激素过多所致的胰岛素抵抗应被解释为胰岛素细胞机制在胰岛素受体远端某一步骤的改变。胰岛素与受体结合增加可能是由受体后事件调节的。
