Coxe J S, O'Dorisio T M, Cataland S, Crockett S E
J Clin Endocrinol Metab. 1981 May;52(5):1002-5. doi: 10.1210/jcem-52-5-1002.
We studied gastric inhibitory peptide (GIP) in response to a mixed meal in both adult-onset diabetics and normal controls. The adult-onset diabetic group was also studied for immunoreactive GIP (IR-GIP), insulin, and glucose with a test meal before and after tolazamide therapy. Mean basal and meal-stimulated IR-GIP concentrations were greater (P less than 0.05) in the adult-onset diabetic group than in normal controls. With treatment, mean fasting glucose significantly decreased (P less than 0.05) from 206 +/- 14 to 162 +/- 11 mg/dl, and postprandial glucose concentrations were reduced (P less than 0.05) between 5-180 min. In contrast, after 1 month of treatment with tolazamide, IR-GIP concentrations were not significantly altered. Further, basal and postmeal serum insulin levels were significantly higher (P less than 0.05) after tolazamide therapy. We conclude that the enteroinsular axis in terms of IR-GIP is overactive in adult-onset diabetics; tolazamide therapy does not appear to effect its meal-stimulated response.
我们研究了成年发病型糖尿病患者和正常对照者对混合餐的胃抑制肽（GIP）反应。还对成年发病型糖尿病组在甲苯磺丁脲治疗前后进行了试验餐的免疫反应性GIP（IR-GIP）、胰岛素和葡萄糖研究。成年发病型糖尿病组的平均基础和餐刺激IR-GIP浓度高于正常对照组（P<0.05）。治疗后，平均空腹血糖从206±14显著降至162±11mg/dl（P<0.05），餐后5-180分钟的血糖浓度降低（P<0.05）。相比之下，甲苯磺丁脲治疗1个月后，IR-GIP浓度无显著变化。此外，甲苯磺丁脲治疗后基础和餐后血清胰岛素水平显著升高（P<0.05）。我们得出结论，在成年发病型糖尿病患者中，就IR-GIP而言，肠胰岛轴过度活跃；甲苯磺丁脲治疗似乎不影响其餐刺激反应。
