Role of phospholipase and calmodulin inhibitors on insulin, arachidonic acid and prostaglandin E2 release.
Role of phospholipase and calmodulin inhibitors on insulin, arachidonic acid and prostaglandin E2 release.
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磷脂酶和钙调蛋白抑制剂对胰岛素、花生四烯酸和前列腺素 E2 释放的作用。
DOI：
10.1016/s0168-8227(86)80045-6
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发表时间：
1985
影响因子：
5.1
通讯作者：
M. García
中科院分区：
文献类型：
--
作者：
J. Gagliardino;M. Borelli;E. D. de Gagliardino;M. García
采用多种实验方法，同时研究了葡萄糖对大鼠胰岛分泌胰岛素、花生四烯酸和前列腺素E2的影响。16.6 mmol/l葡萄糖浓度刺激胰岛素、花生四烯酸和胰高血糖素的释放。所有这些影响都显着降低钙调素和磷脂酶A2抑制剂，或省略钙的孵育介质。磷脂酶A2抑制剂不改变葡萄糖诱导的胰岛净45 Ca ~（2+）摄取。我们的研究结果表明，激活磷脂酶，特别是A2，参与葡萄糖刺激胰岛素释放的机制。这种激活增加了细胞内花生四烯酸、胰高血糖素和可能的磷脂降解产物的浓度，其可以作为胰岛素刺激-分泌偶联的信使。钙-钙调素复合物参与了这一作用。相反，葡萄糖诱导的胰岛净钙摄取可能是之前的磷脂酶激活或不显着影响其活性的封锁。
Using several experimental approaches, we have studied simultaneously the effect of glucose upon insulin, arachidonic acid and prostaglandin E2release by rat pancreatic islets. A 16.6 mmol/l glucose concentration stimulated the release of insulin, arachidonic acid and prostaglandins. All these effects were significantly reduced either by calmodulin and phospholipase A2inhibitors, or by the omission of calcium in the incubation medium. Phospholipase A2inhibitors do not modify the glucose-induced net45Ca2+uptake by isolated islets. Our results would suggest that activation of phospholipases, particularly A2, is involved in the mechanism by which glucose stimulates insulin release. This activation increases the intracellular concentration of arachidonic acid, prostaglandins and probably phospholipid degradation products, that could act as messengers for the stimulus-secretion coupling of insulin. The calcium-calmodulin complex would take part in this effect. Conversely, the glucose-induced net calcium uptake by the islets might either be preceded by phospholipase activation or not significantly affected by the blockade of its activity.
大鼠胰岛中磷酸肌醇反应的底物要求。
DOI：
10.1016/0304-4165(81)90340-8
发表时间：
1981
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
ClementsJr,RS;Evans,MH;Pace,CS
通讯作者：
Pace,CS