ARACHIDONYLTRIFLUOROMETHYL KETONE ON CYTOSOLIC [CA2+] IN HIT INSULINOMA CELLS

D-葡萄糖对胰岛的刺激作用 非酯化花生四烯酸的磷脂水解和积累 酸，如同位素稀释质谱仪所证明的。类似 这些事件发生在HIT胰岛素瘤细胞中，积累的 花生四烯酸可能参与葡萄糖诱导的胰岛β细胞 (Ca2+)。催化的磷脂酶的同一性 葡萄糖诱导的β细胞磷脂的水解性尚不清楚。 AA类似物ATFMK抑制85 kDa胞浆磷脂酶 A2酶。ATFMK对HIT胰岛素瘤细胞的作用 胞浆[Ca~(2+)]迟发性、持续性和不可逆性升高 所需的细胞外钙离子，以及浓度依赖的抑制 去极化引起的胞浆[Ca~(2+)]升高 对AFTMK的延迟反应开始。这些结果表明， ATFMK对钙动员的干扰作用可能 这在一定程度上与其对(-Ce)分泌胰岛素的影响有关 LLS。

Stimulation of pancreatic islets with D-glucose induces phospholipid hydrolysis and accumulation of non-esterified arachidonic acid, as demonstrated by isotope dilution mass spectrometry. Similar events occur in HIT insulinoma cells, and the accumulation of arachidonate may participate in the glucose-induced in beta cell (Ca2+]. The identity of the phospholipase enzyme which catalyzes glucose-induced hydrolysis of beta cell phospholipids is not known. ATFMK, an analogue of AA, inhibits an 85 kDa cytosolic phospholipase A2 enzyme. Exposure of HIT insulinoma cells to ATFMK induced a delayed, sustained, and irreversible increase in cytosolic [Ca2+] that required extracellular Ca2+, and a concentration-dependent inhibition of depolarization-induced increases in cytosolic [Ca2+], prior to onset of the delayed response to AFTMK. These results suggest a disruptive effect of ATFMK on calcium mobilization which may contribute, in part, to its effects on insulin secretion from (-ce lls.