Suthijumroon A, Toth E L, Crockford P M, Ryan E A
Department of Medicine, University of Alberta, Edmonton.
Clin Invest Med. 1988 Dec;11(6):435-40.
We have assessed insulin action in five hyperthyroid patients, pre- and post-radioactive iodine therapy using oral glucose tolerance tests, monocyte insulin binding and dose response curves generated with the euglycemic clamp technique. All patients had become euthyroid after radioactive iodine therapy with a decline in the plasma free T4 index level from 278 +/- 43 to 105 +/- 9. Fasting glucose was modestly, but significantly elevated in the thyrotoxic patients compared to when they were rendered euthyroid (p less than 0.05). Oral glucose tolerance tests showed no difference in either glucose or insulin values after the glucose load. Insulin receptor binding and affinity were similar regardless of their thyroid status. Hepatic glucose production in the basal state was elevated in the thyrotoxic patients, 61 +/- 5 mg/M2/min vs 49 +/- 3 mg/M2/min (p less than 0.05). At the lowest level of insulin infusion no difference in glucose disposal was found. At maximum insulin concentrations the glucose disposal rate was enhanced in the thyrotoxic patients, 686 +/- 19 vs 567 +/- 26 mg/M2/min (p less than 0.01). These results indicate that higher fasting glucose levels may result from increased hepatic glucose production in thyrotoxicosis, but as indicated by the oral glucose tolerance tests, this defect in insulin action is usually of minor significance. However, insulin responsiveness measured at pharmacological insulin levels is augmented in thyrotoxicosis.
我们利用口服葡萄糖耐量试验、单核细胞胰岛素结合以及采用正常血糖钳夹技术生成的剂量反应曲线,评估了5例甲状腺功能亢进患者在放射性碘治疗前后的胰岛素作用。放射性碘治疗后所有患者均恢复正常甲状腺功能,血浆游离T4指数水平从278±43降至105±9。与恢复正常甲状腺功能后相比,甲状腺毒症患者的空腹血糖略有升高,但差异有统计学意义(p<0.05)。口服葡萄糖耐量试验显示,葡萄糖负荷后葡萄糖或胰岛素值无差异。无论甲状腺状态如何,胰岛素受体结合和亲和力均相似。甲状腺毒症患者基础状态下的肝葡萄糖生成增加,为61±5mg/M2/min,而正常甲状腺功能患者为49±3mg/M2/min(p<0.05)。在最低胰岛素输注水平时,未发现葡萄糖处置有差异。在最大胰岛素浓度时,甲状腺毒症患者的葡萄糖处置率增加,为686±19mg/M2/min,而正常甲状腺功能患者为567±26mg/M2/min(p<0.01)。这些结果表明,甲状腺毒症时空腹血糖水平升高可能是由于肝葡萄糖生成增加所致,但正如口服葡萄糖耐量试验所示,这种胰岛素作用缺陷通常意义不大。然而,在药理学胰岛素水平下测得的胰岛素反应性在甲状腺毒症时增强。