Tanigawa K, Kashiwada J, Tamura K, Kawaguchi M, Seino Y, Kato Y
Department of Internal Medicine, Shimane Medical University, Japan.
Diabetes Res. 1994;26(1):1-11.
We compared insulin secretory activity from rat pancreatic islets with that from a hamster beta-cell line (HIT-T). Insulin release from HIT cells was maximally stimulated with glucose at a concentration of 11.1 mM, and rather inhibited by higher concentrations of glucose. Blunted insulin release induced by glucose was shown in the isolated rat islets exposed to either streptozotocin (2.2 mM) for 30 min or alloxan (2 mM) for 5 min, whereas glucose-induced insulin release from HIT cells was not affected by pre-treatment with such beta-cell toxin. When pancreatic islets and HIT cells were cultured for 7 days with 10 mM nicotinamide, an inhibitor of poly (ADP-ribose) synthetase, glucose-induced insulin release from the islets was inhibited, whereas insulin release from HIT cells was rather enhanced. Insulin release induced by either arginine or leucine was also enhanced in HIT cells cultured with nicotinamide. These findings indicate that the multiple components of insulin stimulus-secretion coupling in HIT cells are considerably different from those in rat pancreatic islets.
我们比较了大鼠胰岛与仓鼠β细胞系（HIT-T）的胰岛素分泌活性。HIT细胞的胰岛素释放在葡萄糖浓度为11.1 mM时受到最大刺激，而更高浓度的葡萄糖则对其有抑制作用。在暴露于链脲佐菌素（2.2 mM）30分钟或四氧嘧啶（2 mM）5分钟的分离大鼠胰岛中，葡萄糖诱导的胰岛素释放减弱，而HIT细胞中葡萄糖诱导的胰岛素释放不受此类β细胞毒素预处理的影响。当胰岛和HIT细胞用10 mM烟酰胺（一种聚（ADP-核糖）合成酶抑制剂）培养7天时，葡萄糖诱导的胰岛胰岛素释放受到抑制，而HIT细胞的胰岛素释放反而增强。在用烟酰胺培养的HIT细胞中，精氨酸或亮氨酸诱导的胰岛素释放也增强。这些发现表明，HIT细胞中胰岛素刺激-分泌偶联机制的多个组成部分与大鼠胰岛中的有很大不同。
