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目的 探讨GLP -1(7-36 )NH2 促胰岛素分泌的细胞内机制。方法 用放免法检测GLP -1(7-36 )NH2 在不同葡萄糖浓度下对培养的新生大鼠胰岛 β细胞的胰岛素分泌量和cAMP含量的变化。 结果 在 2 .8mmol/L葡萄糖时 ,GLP -1(7-36 )NH2 使 β细胞胰岛素分泌和cAMP含量无明显增加 ;优降糖能使胰岛素分泌增加 ,而cAMP含量无明显变化。在 5 .6 ,11.2和 16 .7mmol/L葡萄糖时 ,GLP -1(7-36 )NH2 使胰岛素分泌和cAMP含量均明显增加。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 ,但仍使cAMP含量增加。结论 GLP -1(7-36 )NH2 具有葡萄糖浓度依赖的刺激cAMP生成的作用 ,β细胞内cAMP含量增加是其引起胰岛素释放的关键环节
Objective To investigate the intracellular mechanism of GLP-1 (7-36) NH2-induced insulin secretion. Methods The changes of insulin secretion and cAMP content in islet β cells of cultured neonatal rat GLP-1 (7-36) NH2 were detected by radioimmunoassay at different glucose concentrations. Results When GLP-1 (7-36) NH2 was added at 2. 8mmol / L glucose, β-cell insulin secretion and cAMP content did not increase significantly. Glutamine increased insulin secretion but cAMP content did not change significantly. At 5.6, 11.2 and 16.7 mmol / L glucose, GLP-1 (7-36) NH2 markedly increased both insulin secretion and cAMP content. At 16.7 mmol / L glucose, GLP-1 (7-36) NH2 failed to induce insulin secretion but still increased cAMP levels after the addition of EGTA or nifedipine. Conclusion GLP-1 (7-36) NH2 has the effect of stimulating cAMP production in a concentration-dependent manner. The increase of cAMP content in β-cells is a key factor that leads to the release of insulin