Calcium and pancreatic beta-cell function. 12. Modification of 45Ca fluxes by excess of K+.
Calcium and pancreatic beta-cell function. 12. Modification of 45Ca fluxes by excess of K+.
复制标题
钙和胰腺 β 细胞功能。
DOI：
10.1530/acta.0.0960087
复制
发表时间：
1981
期刊：
影响因子：
--
通讯作者：
B. Hellman
中科院分区：
文献类型：
--
作者：
T. Andersson;C. Betsholtz;B. Hellman
胰岛素释放的葡萄糖刺激被认为是由于胰腺β细胞的去极化以及随后的Ca 2+内流。采用来自非近交系ob/ob小鼠的分离的胰岛来阐明葡萄糖对β细胞处理Ca 2+的影响是否可以通过过量K+诱发的去极化来模拟。添加25 mM K+与20 mM葡萄糖在刺激细胞内摄取45 Ca方面一样有效。在这两种情况下，额外量的纳入45 Ca出现在线粒体和分泌颗粒。当分析45 Ca的洗脱模式时，很明显，提高K+的效果不同于葡萄糖引起的效果。而葡萄糖抑制45 Ca流出与Ca ~（2+）缺乏的培养基灌流过程中，K+的加入导致轻微的刺激。此外，45 Ca纳入响应K+更容易动员。
Glucose stimulation of insulin release is supposed to result from depolarization of the pancreatic beta-cells with subsequent influx of Ca2+. Isolated islets from non-inbred ob/ob-mice were employed for elucidating whether the glucose effects on the beta-cell handling of Ca2+ could be simulated by the depolarization evoked by excess of K+. Addition of 25 mM K+ was as effective as 20 mM glucose in stimulating the intracellular uptake of 45Ca. In both instances the additional amounts of incorporated 45Ca appeared in the mitochondria and the secretory granules. When analysing the washout pattern for 45Ca it was evident that the effects of raising K+ differed from those evoked by glucose. Whereas glucose inhibited 45Ca efflux during perifusion with Ca2+-deficient medium the addition of K+ resulted in a slight stimulation. Furthermore, the 45Ca incorporated in response to K+ was more readily mobilised.