EFFECTS OF GLUCOSE ON CA-45(2+) OUTFLOW, CYTOSOLIC CA-2+ CONCENTRATION AND INSULIN RELEASE FROM FRESHLY ISOLATED AND CULTURED ADULT-RAT ISLETS

被引:17
作者
BOSCHERO, AC
BORDIN, S
HERCHUELZ, A
LEBRUN, P
机构
[1] FREE UNIV BRUSSELS,SCH MED,PHARMACOL LAB,115 BLD WATERLOO,B-1000 BRUSSELS,BELGIUM
[2] UNIV ESTADUAL CAMPINAS,INST BIOL,DEPT PHYSIOL & BIOPHYS,BR-13100 CAMPINAS,SP,BRAZIL
基金
巴西圣保罗研究基金会;
关键词
D O I
10.1016/0143-4160(90)90015-M
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The present study aimed at comparing the effects of glucose on ionic and secretory events in freshly isolated and 5-7 day cultured rat pancreatic islets. The capacity of glucose to provoke insulin release was severely reduced in islets maintained in culture. Whether in freshly isolated or cultured islets, glucose provoked a marked and sustained decrease in 45Ca2+ outflow from islets deprived of extracellular Ca2+. In the presence of extracellular Ca2+ throughout, the magnitude of the glucose-induced secondary rise in 45Ca2+ outflow was reduced in cultured islets. Glucose provoked a weaker increase in [Ca2+]i in islet cells obtained from cultured islets than in islet cells dissociated from freshly isolated pancreatic islets. On the other hand, the stimulatory effect of carbamylcholine on 45Ca2+ outflow was unaffected by tissue culture. Lastly, in islet cells obtained from cultured islets, the increase in [Ca2+]i evoked by K+ depolarization averaged half of that observed in control experiments. These results indicate that the reduced secretory potential of glucose in cultured pancreatic islets can be ascribed to the inability of the nutrient secretagogue to provoke a suitable increase in Ca2+ influx. © 1990.
引用
收藏
页码:603 / 609
页数:7
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