Draznin B, Kao M, Sussman K E
Diabetes. 1987 Feb;36(2):174-8. doi: 10.2337/diab.36.2.174.
We investigated the effect of insulin and a hypoglycemic sulfonylurea agent glyburide on cytosolic free-Ca2+ concentrations [( Ca2+]i) in isolated rat adipocytes. Both insulin and glyburide increased [Ca2+]i in a dose-dependent manner. Half-maximal effects were seen at 0.5 ng/ml of insulin and 0.5 microM glyburide. Nifedipine (25 microM), a Ca2+-channel blocker, inhibited the effect of both agents. The effect of insulin on [Ca2+]i was 40 and 70% potentiated by ambient glucose concentrations at 180 and 300 mg/dl, respectively. Depolarizing doses of potassium (40 mM) induced an increase in cytosolic Ca2+ that was also inhibited by nifedipine. It is suggested that both insulin and glyburide increase cytosolic free Ca2+ levels at least in part by promoting Ca2+ influx through voltage-dependent Ca2+ channels.
我们研究了胰岛素和降糖磺脲类药物格列本脲对分离的大鼠脂肪细胞胞浆游离钙离子浓度[Ca2+]i的影响。胰岛素和格列本脲均以剂量依赖方式增加[Ca2+]i。胰岛素浓度为0.5 ng/ml和格列本脲浓度为0.5 microM时可观察到半数最大效应。钙通道阻滞剂硝苯地平（25 microM）可抑制这两种药物的作用。环境葡萄糖浓度分别为180和300 mg/dl时，胰岛素对[Ca2+]i的作用分别增强40%和70%。去极化剂量的钾（40 mM）可诱导胞浆钙离子增加，这也被硝苯地平抑制。提示胰岛素和格列本脲至少部分通过促进钙离子经电压依赖性钙通道内流来增加胞浆游离钙离子水平。
