Secretagogue-induced diacylglycerol accumulation in isolated pancreatic islets. Mass spectrometric characterization of the fatty acyl content indicates multiple mechanisms of generation.
Secretagogue-induced diacylglycerol accumulation in isolated pancreatic islets. Mass spectrometric characterization of the fatty acyl content indicates multiple mechanisms of generation.
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促分泌素诱导的二酰甘油在离体胰岛中积累。
DOI：
10.1021/bi00436a026
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发表时间：
1989
期刊：
影响因子：
2.9
通讯作者：
Turk,J
中科院分区：
文献类型：
--
作者：
Wolf,BA;Easom,RA;Hughes,JH;McDaniel,ML;Turk,J
2月7日收到修订稿摘要：用一种新发展的负离子化学电离质谱法检测了二酰甘油在促分泌剂刺激的胰岛中的蓄积。卡巴胆碱激动剂卡巴胆碱可诱导富含花生四烯酸和硬脂酸的二酰甘油在胰岛中积聚，并在预先标记了[~H]甘油的卡巴胆碱刺激的胰岛中平行积聚~3H标记的二甘油。这样标记的胰岛不会因D-葡萄糖而累积~3H标记的二酰甘油，但D-葡萄糖确实会诱导胰岛质量分数的二酰甘油积累。这种物质富含棕榈酸和油酸，而花生四烯酸的含量要少得多。这两种促分泌剂都不影响三酰甘油的标记，也不能诱导预先标记[~3H]胆碱的胰岛释放[~3H]胆碱或[~3H]磷胆碱。这些观察表明，在胰岛中积累的二酰甘油是由甘油脂的水解产生的，可能包括磷脂酰肌醇。对葡萄糖的反应而积累的甘油二酯的大部分不是由甘油脂水解产生的，因此必须反映从头合成。内源性甘油二酯可能参与了胰岛素的分泌，因为外源性甘油二酯可诱导胰岛分泌胰岛素，而二酰甘油代谢为磷脂酸的抑制剂可增加葡萄糖诱导的胰岛素分泌。
Revised Manuscript Received February 7, 1989 abstract: Diacylglycerol accumulation has been examined in secretagogue-stimulated pancreatic islets with a newly developed negative ion chemical ionization mass spectrometric method. The muscarinic agonist carbachol induces islet accumulation of diacylglycerol rich in arachidonate and stearate, and a parallel accumulation of 3H-labeled diacylglycerol occurs in carbachol-stimulated islets that had been prelabeled with [3H] glycerol. Islets so labeled do not accumulate 3H-labeled diacylglycerol in response to D-glucose, but D-glucose does induce islet accumulation of diacylglycerol by mass. This material is rich in palmitate and oleate and contains much smaller amounts of arachidonate. Neither secretagogue influences tri-acylglycerol labeling, and neither inducesrelease of [3H] choline or [3H] phosphocholine from islets prelabeled with [3H] choline. These observations indicate that the diacylglycerol that accumulates in islets in response to carbachol arises from hydrolysis of glycerolipids, probably including phosphoinositides. The bulk of the diacylglycerol which accumulates in response to glucose does not arise from glycerolipid hydrolysis and must therefore reflect de novo synthesis. The endogenous diacylglycerol which accumulates insecretagoguestimulated islets mayparticipate in insulin secretionbecause exogenous diacylglycerol induces insulin secretion from islets, and an inhibitor of diacylglycerolmetabolism to phosphatidic acid augments glucose-induced insulin secretion.