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目的 :探讨GLP - 1(7- 36 )NH2 促胰岛素分泌的机制。方法 :以DiBAC4 (3)为探针 ,用粘附式细胞仪研究GLP - 1(7- 36 )NH2 对培养的新生大鼠胰岛 β细胞膜电位的作用 ,并用放免法检测GLP - 1(7- 36 )NH2在不同葡萄糖浓度下引起的胰岛素分泌量的变化。结果 :在 2 8mmol/L葡萄糖时 ,GLP - 1(7- 36 )NH2 使 β细胞胰岛素分泌无明显增加 ,β细胞膜电位无明显变化 ;在 5 6、16 7mmol/L葡萄糖时 ,GLP - 1(7- 36 )NH2 使胰岛素分泌明显增加 ,它能增强葡萄糖引起的 β细胞膜去极化反应。在 16 7mmol/L葡萄糖时 ,加入EGTA或硝苯吡啶后 ,GLP - 1(7- 36 )NH2 不能引起胰岛素分泌 ,β细胞膜也无去极化反应。 结论 :GLP - 1(7- 36 )NH2 具有葡萄糖浓度依赖的促胰岛素释放作用 ,它能增强葡萄糖引起的 β细胞去极化反应。
Objective: To investigate the mechanism of GLP - 1 (7-36) NH2 insulin secretion. Methods: The effect of GLP - 1 (7-36) NH2 on the islet β cell membrane potential of cultured neonatal rat was studied by using adherent cytometer with DiBAC4 (3) as probe. The level of GLP - 1 36) Changes in the amount of insulin secreted by NH2 at different glucose concentrations. Results GLP - 1 (7-36) NH2 showed no significant increase in insulin secretion and no significant change in β cell membrane potential at 28 mmol / L glucose. When GLP - 1 (7-36) 7-36) NH2 significantly increased insulin secretion, it can enhance the glucose-induced β cell membrane depolarization. GLP - 1 (7-36) NH2 did not induce insulin secretion when added with EGTA or nifedipine at 16 7mmol / L glucose, and no depolarization occurred in β - cell membrane. CONCLUSION: GLP - 1 (7-36) NH2 has a glucose - dependent insulinotropic effect and enhances glucose - induced depolarization of β cells.