Billaudel B, Mathias P C, Sutter B C, Malaisse W J
J Endocrinol. 1984 Feb;100(2):227-33. doi: 10.1677/joe.0.1000227.
Corticosterone (0.6 mumol/l) inhibited both 45Ca outflow and insulin release evoked by glucose, the combination of leucine and glutamine, 2-ketoisocaproate, gliclazide or the association of gliclazide and a tumour-promoting phorbol ester in rat pancreatic islets perifused at normal extracellular Ca2+ concentration (1.0 mmol/l). In all cases, the inhibitory action of corticosterone reached statistical significance within 10-22 min of exposure to this steroid and failed to be rapidly reversible. Corticosterone failed to affect basal 45Ca outflow and insulin release. The steroid also failed to affect the inhibitory action of glucose upon 45Ca outflow, as judged from either the glucose-induced early fall in effluent radioactivity from islets maintained at normal extracellular Ca2+ concentration or the steady-state values for 45Ca outflow from glucose-stimulated but Ca2+-deprived islets. Corticosterone caused a modest increase in 86Rb outflow from islets perifused in the presence of glucose (16.7 mmol/l). It is concluded that corticosterone impairs Ca2+ inflow into the islet cells and, by doing so, causes a progressive inhibition of insulin release. The pancreatic B cell might thus serve as a further model for the study of the rapid biological response to steroids, as presumably mediated by alteration in the biophysical properties of the plasma membrane.
在正常细胞外钙离子浓度（1.0 mmol/L）下灌流的大鼠胰岛中，皮质酮（0.6 μmol/L）抑制了由葡萄糖、亮氨酸与谷氨酰胺组合、2-酮异己酸、格列齐特或格列齐特与促肿瘤佛波酯联合引发的45Ca外流及胰岛素释放。在所有情况下，皮质酮的抑制作用在接触该类固醇10 - 22分钟内达到统计学显著水平，且不能迅速逆转。皮质酮未能影响基础45Ca外流及胰岛素释放。从维持在正常细胞外钙离子浓度的胰岛流出放射性物质中葡萄糖诱导的早期下降，或从葡萄糖刺激但钙离子缺失的胰岛45Ca外流的稳态值判断，该类固醇也未能影响葡萄糖对45Ca外流的抑制作用。皮质酮使在葡萄糖（16.7 mmol/L）存在下灌流的胰岛中86Rb外流适度增加。结论是皮质酮损害钙离子流入胰岛细胞，进而导致胰岛素释放的逐渐抑制。胰腺β细胞可能因此成为研究类固醇快速生物学反应的另一个模型，这种反应大概是由质膜生物物理特性的改变介导的。
