Gylfe E, Hellman B
Biochim Biophys Acta. 1978 Jan 18;538(2):249-57. doi: 10.1016/0304-4165(78)90353-7.
beta-Cell-rich pancreatic islets were microdissected from ob/ob-mice and loaded with 45Ca in the presence of 3 or 20 mM glucose. Subsequent measurements of the effluxes of radioactivity in a perifusion apparatus revealed that the slowly exchangeable 45Ca taken up in response to glucose was also preferentially mobilised by this compound. Glucose stimulation of 45Ca efflux was abolished after omission of calcium from the perifusion medium but persisted when insulin release was inhibited by prolonged starvation, addition of L-epinephrine or lowering of temperature. The presence of a stimulated efflux of radioactivity even under conditions of inhibited insulin release indicates that sources other than beta-granules ejected by exocytosis contribute to the additional 45Ca released after raising the glucose concentration of the perifusion medium. It is suggested that the beta-cell depolarisation as such may account for part of the 45Ca mobilised by glucose.
富含β细胞的胰岛从ob/ob小鼠中显微分离出来,并在3或20 mM葡萄糖存在的情况下加载45Ca。随后在灌流装置中对放射性流出进行测量,结果显示,响应葡萄糖摄取的可缓慢交换的45Ca也优先被该化合物动员。从灌流培养基中去除钙后,葡萄糖刺激的45Ca流出被消除,但当胰岛素释放因长期饥饿、添加L-肾上腺素或降低温度而受到抑制时,这种刺激仍然持续。即使在胰岛素释放受到抑制的条件下,放射性流出仍受到刺激,这表明除了通过胞吐作用排出的β颗粒之外的其他来源,也对提高灌流培养基葡萄糖浓度后释放的额外45Ca有贡献。有人提出,β细胞去极化本身可能是葡萄糖动员的部分45Ca的原因。