ROLES OF INSULIN-RESISTANCE AND BETA-CELL DYSFUNCTION IN THE PATHOGENESIS OF GLUCOSE-INTOLERANCE IN CYSTIC-FIBROSIS
ROLES OF INSULIN-RESISTANCE AND BETA-CELL DYSFUNCTION IN THE PATHOGENESIS OF GLUCOSE-INTOLERANCE IN CYSTIC-FIBROSIS
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DOI：
10.1210/jc.79.1.80
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发表时间：
1994-07-01
影响因子：
5.8
通讯作者：
ARSLANIAN, S
中科院分区：
文献类型：
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作者：
AUSTIN, A;KALHAN, SC;ARSLANIAN, S
在8例（年龄16.5 +/- 1.9岁）、4例糖耐量正常（NGT）和4例糖耐量受损（IGT）患者以及7例健康对照（CN）受试者中，评估了胰岛素缺乏和胰岛素抵抗在囊性纤维化（CF）中葡萄糖耐受不良发病机制中的作用。在高血糖钳夹期间评估第一和第二阶段胰岛素分泌。使用[6,6- h -2(2)]葡萄糖和逐步高胰岛素-正血糖钳测量肝葡萄糖生成（HGP）和胰岛素刺激的葡萄糖处置。两组CF患者的一期和二期胰岛素水平均显著低于对照组。糖蛋白水平与一期胰岛素（r = -0.81, P = 0.015）、二期胰岛素（r = -0.97, P < 0.001）呈负相关。在高血糖钳夹期间，与对照值（6.66 +/- 1.79、12.82 +/- 1.61和13.02 +/- 1.78 mu mol/kg.min/pmol）相比，CF-IGT的胰岛素敏感性指数降低，而CF-NGT则没有降低。L分别;P < 0.05)。CF组基础HGP和空腹血糖高于CN组[24.8 +/- 2.9 vs. 16.9 +/- 1.4 mu mol/kg]。min （P = 0.036）和5.8±0.2 us。5.4 +/- 0.1 mmol/L （P = 0.035）。在高胰岛素正糖钳夹期间，胰岛素刺激的葡萄糖处置在CF-IGT （45.68 +/- 4.87 mu mol/kg min）显著低于CF-NGT （78.99 +/- 1.34 mu mol/kg）。CN （71.74 +/- 6.88 mu mol/kg.min）。CF-IGT组胰岛素敏感性低于CF-NGT组（7.04 +/- 0.86和14.38 +/- 0.84 mu mol/kg.min/pmol.L; P < 0.05）。我们得出结论：1)血红蛋白与CF患者胰岛素缺乏密切相关；2)这组CF患者的葡萄糖耐受不良是胰岛素缺乏和胰岛素抵抗的结果。
The roles of insulin deficiency and insulin resistance in the pathogenesis of glucose intolerance in cystic fibrosis (CF) were evaluated in eight patients (aged 16.5 +/- 1.9 yr), four with normal glucose tolerance (NGT) and four with impaired glucose tolerance (IGT), and in seven healthy control (CN) subjects. First and second phase insulin secretions were evaluated during a hyperglycemic clamp. Hepatic glucose production (HGP) and insulin-stimulated glucose disposal were measured using [6,6-H-2(2)]glucose and a stepwise hyperinsulinemic-euglycemic clamp.First and second phase insulin levels were significantly lower in both groups of CF patients compared with control values. There was an inverse relationship between glycohemoglobin level and first phase insulin (r = -0.81; P = 0.015) and second phase insulin (r = -0.97; P < 0.001). During the hyperglycemic clamp, the insulin sensitivity index was lower in CF-IGT, but not CF-NGT, compared with control values (6.66 +/- 1.79, 12.82 +/- 1.61, and 13.02 +/- 1.78 mu mol/kg.min/pmol.L, respectively; P < 0.05).Basal HGP and fasting plasma glucose were higher in CF vs. CN [24.8 +/- 2.9 vs. 16.9 +/- 1.4 mu mol/kg.min (P = 0.036) and 5.8 +/- 0.2 us. 5.4 +/- 0.1 mmol/L (P = 0.035), respectively]. During the hyperinsulinemic euglycemic clamp, insulin-stimulated glucose disposal was significantly lower in CF-IGT (45.68 +/- 4.87 mu mol/kg min) vs. CF-NGT (78.99 +/- 1.34 mu mol/kg.min) and CN (71.74 +/- 6.88 mu mol/kg.min). Insulin sensitivity was lower in CF-IGT vs. CF-NGT (7.04 +/- 0.86 and 14.38 +/- 0.84 mu mol/kg.min/pmol.L; P < 0.05).We conclude that 1) glycohemoglobin is a strong correlate of insulin deficiency in CF; and 2) glucose intolerance in this group of CF patients occurred as a consequence of concomitant insulin deficiency and insulin resistance.