Landgraf R, Landgraf-Leurs M M
Prostaglandins. 1979 Apr;17(4):599-613. doi: 10.1016/0090-6980(79)90011-x.
Using the isolated perfused rat pancreas PGE2 (1 MUM and 10 muM) had no effect on basal or glucose (10 and 20 mM)-induced insulin release (IR). PGF2 alpha stimulated basal IR at 1 muM and inhibited IR at 10 muM. The glucose-induced IR was unaffected by this PG. Furosemide (5 and 10 mM) led to a monophastic IR at low glucose (glu) and to a potentiation of IR at high glu. Only high indomethacin (Indo) (50 microgram/ml) inhibited glu-induced IR. The stimulatory effect of furosemide on IR could not be inhibited by indomethacin. However mepacrine (0.1 mM) abolished the furosemide effect. Also glu-induced IR was inhibited by mepacrine. Acetylsalicylic acid (30 mg/100 ml) had no significant influence on glu-induced IR. These findings provide evidence that phospholipase activation rather than increased PG synthesis might primarily be involved in the secretory process of insulin.
使用离体灌注大鼠胰腺，前列腺素E2（1微摩尔和10微摩尔）对基础或葡萄糖（10和20毫摩尔）诱导的胰岛素释放（IR）没有影响。前列腺素F2α在1微摩尔时刺激基础胰岛素释放，在10微摩尔时抑制胰岛素释放。葡萄糖诱导的胰岛素释放不受这种前列腺素的影响。速尿（5和10毫摩尔）在低糖时导致单相胰岛素释放，在高糖时增强胰岛素释放。只有高剂量的消炎痛（50微克/毫升）抑制葡萄糖诱导的胰岛素释放。消炎痛不能抑制速尿对胰岛素释放的刺激作用。然而，米帕林（0.1毫摩尔）消除了速尿的作用。米帕林也抑制葡萄糖诱导的胰岛素释放。乙酰水杨酸（30毫克/100毫升）对葡萄糖诱导的胰岛素释放没有显著影响。这些发现提供了证据，表明磷脂酶激活而非前列腺素合成增加可能主要参与胰岛素的分泌过程。
