Ammon H P, Abdel-hamid M
Naunyn Schmiedebergs Arch Pharmacol. 1981 Nov;317(3):262-7. doi: 10.1007/BF00503828.
It has been suggested that the islet thiol redox status plays a role in the regulation of beta-cell sensitivity in response to insulin secretagogues. Employing the isolated perfused rat pancreas, the effect of reduced glutathione (1 mM) and L-cysteine (5 mM) on insulin release induced by tolbutamide (0.2 mg/ml), glucose (5.6 and 11.1 mM) and tolbutamide (0.1 mg/ml) in the presence of 5.6 mM glucose was studied. In the absence of glucose or in the presence of 5.6 mM of glucose neither glutathione nor L-cysteine stimulated the release of insulin. Reduced glutathione potentiated the secretion induced by glucose (11.1 mM) during the first and the second phase. L-Cysteine potentiated only the first phase of glucose-induced insulin release, whereas the second phase was depressed. Both of the tested thiols potentiated the insulin secretory action of either tolbutamide (0.2 mg/ml) alone or tolbutamide (01. mg/ml) in the presence of glucose (5.6 mM). The data suggest that supplementation of thiols to the pancreatic beta-cells perse cannot initiate the insulin secretory process. It is also suggested that GSH and L-cysteine increase the sensitivity of beta-cells to the stimulatory action of tolbutamide and/or glucose.
有人提出，胰岛硫醇氧化还原状态在调节β细胞对胰岛素促分泌剂的敏感性中起作用。利用离体灌注大鼠胰腺，研究了还原型谷胱甘肽（1 mM）和L-半胱氨酸（5 mM）对甲苯磺丁脲（0.2 mg/ml）、葡萄糖（5.6和11.1 mM）以及在5.6 mM葡萄糖存在下甲苯磺丁脲（0.1 mg/ml）诱导的胰岛素释放的影响。在无葡萄糖或存在5.6 mM葡萄糖的情况下，谷胱甘肽和L-半胱氨酸均未刺激胰岛素释放。还原型谷胱甘肽在第一阶段和第二阶段增强了由葡萄糖（11.1 mM）诱导的分泌。L-半胱氨酸仅增强了葡萄糖诱导的胰岛素释放的第一阶段，而第二阶段则受到抑制。两种测试的硫醇均增强了单独的甲苯磺丁脲（0.2 mg/ml）或在葡萄糖（5.6 mM）存在下甲苯磺丁脲（0.1 mg/ml）的胰岛素分泌作用。数据表明，向胰腺β细胞补充硫醇本身并不能启动胰岛素分泌过程。还表明，谷胱甘肽和L-半胱氨酸增加了β细胞对甲苯磺丁脲和/或葡萄糖刺激作用的敏感性。
