Katayama N, Hughes S J, Persaud S J, Jones P M, Howell S L
Biomedical Sciences Division, King's College London, UK.
Mol Cell Endocrinol. 1995 Jun;111(2):125-8. doi: 10.1016/0303-7207(95)03560-t.
Insulin secretory responses of intact and electrically permeabilised islets of Goto-Kakizaki (GK) rats, a novel model of non-insulin dependent diabetes mellitus, and Wistar (control) rats were compared to investigate the mechanism of the impairment of insulin secretion from pancreatic islets of GK rats. Insulin secretion from intact islets in response to glucose, glyceraldehyde, succinate monomethylester and tetramethyl p-phenylenediamine, which reduces cytochrome c directly, was significantly impaired in GK rats compared to control rats (P < 0.05, P < 0.01, P < 0.05 and P < 0.05, respectively). However, Ca(2+)-induced insulin release from electrically permeabilised islets of GK rats was higher than that of control rats. Moreover, insulin secretion from intact islets in response to 50 mM KCl, which depolarises islet cells, was not impaired in GK rats. These results indicate that insulin secretion from islets of GK rats is not impaired after energy generating steps of metabolism.
比较了非胰岛素依赖型糖尿病新模型——五岛-纪崎（GK）大鼠和Wistar（对照）大鼠完整及电通透胰岛的胰岛素分泌反应，以研究GK大鼠胰岛胰岛素分泌受损的机制。与对照大鼠相比，GK大鼠完整胰岛对葡萄糖、甘油醛、琥珀酸单甲酯和直接还原细胞色素c的四甲基对苯二胺的胰岛素分泌显著受损（分别为P < 0.05、P < 0.01、P < 0.05和P < 0.05）。然而，Ca(2+)诱导的GK大鼠电通透胰岛的胰岛素释放高于对照大鼠。此外，GK大鼠完整胰岛对使胰岛细胞去极化的50 mM KCl的胰岛素分泌未受损。这些结果表明，GK大鼠胰岛在代谢的能量产生步骤后胰岛素分泌未受损。
