Hamdi I, Green M, Shneerson J M, Palmer C R, Hales C N
Department of Clinical Biochemistry, Addenbrooke's Hospital, Cambridge, UK.
Clin Endocrinol (Oxf). 1993 Jul;39(1):21-6. doi: 10.1111/j.1365-2265.1993.tb01746.x.
We determined the changes in insulin, intact proinsulin and 32-33 split proinsulin as markers of beta cell damage in assessing the state of carbohydrate intolerance in patients with cystic fibrosis.
Measurements of insulin, proinsulin and 32-33 proinsulin concentrations in cystic fibrosis following oral glucose tolerance test (OGTT).
Sixteen cystic fibrosis patients attending the chest outpatient clinic for follow-up, age range 14-42 years, and 14 healthy controls matched for age and body mass index.
Insulin, intact proinsulin and 32-33 split proinsulin were measured immunoradiometrically at 0, 30, 60, 90 and 120 minutes after an OGTT. Glucose and HbA1 were also measured.
Cystic fibrosis patients were divided into two groups according to their OGTT results: those with diabetes mellitus or impaired glucose tolerance and those with normal glucose tolerance. Insulin concentrations and insulin/glucose ratios at 30 minutes were lower in both cystic fibrosis groups in comparison with the control. There was also a significant increase in the time to reach peak insulin levels in both cystic fibrosis groups. Fasting intact proinsulin concentrations and the proportion of proinsulin-like molecules were significantly higher in cystic fibrosis with diabetes mellitus or impaired glucose tolerance than in the control group, but not in the normal glucose tolerance cystic fibrosis group. There was no significant difference in the plasma concentrations of 32-33 split proinsulin amongst the three groups.
Abnormal beta cell function in cystic fibrosis patients was reflected initially in a diminished 30-minute insulin response to oral glucose. A significant rise in fasting intact proinsulin and the proportion of proinsulin-like molecules was seen only in cystic fibrosis patients who had progressed to impaired glucose tolerance or diabetes mellitus. Cystic fibrosis patients with normal glucose tolerance showed changes intermediate between the control and the other group.
我们测定了胰岛素、完整胰岛素原和32-33裂解胰岛素原的变化，将其作为评估囊性纤维化患者碳水化合物不耐受状态时β细胞损伤的标志物。
口服葡萄糖耐量试验（OGTT）后测定囊性纤维化患者的胰岛素、胰岛素原和32-33胰岛素原浓度。
16名在胸科门诊接受随访的囊性纤维化患者，年龄范围为14至42岁，以及14名年龄和体重指数匹配的健康对照者。
OGTT后0、30、60、90和120分钟采用免疫放射分析法测定胰岛素、完整胰岛素原和32-33裂解胰岛素原。同时测定血糖和糖化血红蛋白（HbA1）。
根据OGTT结果，囊性纤维化患者分为两组：患有糖尿病或糖耐量受损者以及糖耐量正常者。与对照组相比，两个囊性纤维化组在30分钟时的胰岛素浓度和胰岛素/血糖比值均较低。两个囊性纤维化组达到胰岛素峰值水平的时间也显著延长。患有糖尿病或糖耐量受损的囊性纤维化患者的空腹完整胰岛素原浓度和胰岛素原样分子比例显著高于对照组，但糖耐量正常的囊性纤维化组则不然。三组之间32-33裂解胰岛素原的血浆浓度无显著差异。
囊性纤维化患者的β细胞功能异常最初表现为口服葡萄糖后30分钟胰岛素反应减弱。仅在进展为糖耐量受损或糖尿病的囊性纤维化患者中，空腹完整胰岛素原和胰岛素原样分子比例显著升高。糖耐量正常的囊性纤维化患者的变化介于对照组和另一组之间。
