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新诊断的I型(胰岛素依赖型)糖尿病患者对进餐时免疫反应性胃抑制多肽的反应减弱。

Diminished immunoreactive gastric inhibitory polypeptide response to a meal in newly diagnosed type I (insulin-dependent) diabetics.

作者信息

Krarup T, Madsbad S, Moody A J, Regeur L, Faber O K, Holst J J, Sestoft L

出版信息

J Clin Endocrinol Metab. 1983 Jun;56(6):1306-12. doi: 10.1210/jcem-56-6-1306.

Abstract

The release of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal was examined in 10 normal subjects and 15 type I (insulin-dependent) diabetics 7 days (test I), 14 days (test II), and 3 months (test III) after time of diagnosis. During all three tests, the diabetics had significantly lower plasma IR-GIP concentrations than the controls from 15-90 min after the standard meal. The IR-GIP response in the diabetics measured as the integrated area under the response curve corresponded to 70% of that of normal subjects. beta-cell function evaluated from the C-peptide response to the meal increased significantly from test I to test III whereas the IR-GIP response was similar during all three tests. As GIP is known to potentiate glucose-induced insulin secretion and possibly the biosynthesis of insulin, the low IR-GIP responses in subjects with type I diabetes may significantly influence insulin levels and hyperglycemia.

摘要

在10名正常受试者和15名I型(胰岛素依赖型)糖尿病患者中,于确诊后7天(试验I)、14天(试验II)和3个月(试验III)检测了对标准餐的免疫反应性胃抑制多肽(IR-GIP)释放情况。在所有三项试验中,糖尿病患者在标准餐后15至90分钟时的血浆IR-GIP浓度显著低于对照组。糖尿病患者的IR-GIP反应以反应曲线下的积分面积衡量,相当于正常受试者的70%。从对餐的C肽反应评估的β细胞功能从试验I到试验III显著增加,而IR-GIP反应在所有三项试验中相似。由于已知GIP可增强葡萄糖诱导的胰岛素分泌并可能促进胰岛素的生物合成,I型糖尿病患者中低IR-GIP反应可能会显著影响胰岛素水平和高血糖症。

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