Ding Y, Rana R S
Department of Biological Sciences, St. John's University, Jamaica, New York, 11439, USA.
Biochem Biophys Res Commun. 1998 Oct 29;251(3):699-703. doi: 10.1006/bbrc.1998.9536.
The role of nitric oxide (NO) in glucose-induced insulin secretion was studied in pancreatic beta-cells, HIT-T15. A role for NO is suggested since glucose stimulated NO production in a concentration-dependent manner. NG-monomethyl-L-arginine, a potent inhibitor of nitric oxide synthase, significantly inhibited glucose-induced nitric oxide production as well as insulin release in HIT-T15. Furthermore, this inhibitory effect can be reversed by sodium nitroprusside (SNP), a well known NO donor. While SNP alone did not stimulate insulin release, it potentiated the secretory response of HIT-T15 cells to glucose by approximately two-fold. Potentiation by SNP appears to be mediated by NO, since (i) the potentiation was completely abolished by 10 microM hemoglobin, a scavenger of NO; and (ii) was not affected by rhodanese plus sodium thiosulphate. Neither hemoglobin alone nor the combination of rhodanese and sodium thiosulphate had any effect on glucose induced insulin release. These results are consistent with the hypothesis that glucose-induced formation of NO may potentiate the effect of glucose by a positive feedback mechanism.
在胰腺β细胞HIT-T15中研究了一氧化氮（NO）在葡萄糖诱导的胰岛素分泌中的作用。由于葡萄糖以浓度依赖性方式刺激NO生成，因此提示了NO的作用。NG-单甲基-L-精氨酸是一种有效的一氧化氮合酶抑制剂，它显著抑制HIT-T15中葡萄糖诱导的一氧化氮生成以及胰岛素释放。此外，这种抑制作用可被硝普钠（SNP，一种著名的NO供体）逆转。虽然单独的SNP不会刺激胰岛素释放，但它使HIT-T15细胞对葡萄糖的分泌反应增强了约两倍。SNP的增强作用似乎是由NO介导的，因为：（i）10 microM血红蛋白（一种NO清除剂）完全消除了这种增强作用；（ii）它不受硫氰酸酶加硫代硫酸钠的影响。单独的血红蛋白以及硫氰酸酶和硫代硫酸钠的组合对葡萄糖诱导的胰岛素释放均无任何影响。这些结果与以下假设一致：葡萄糖诱导的NO形成可能通过正反馈机制增强葡萄糖的作用。
