Laychock S G
Mol Pharmacol. 1985 Jan;27(1):66-73.
Rat pancreatic islets methylate phosphatidylethanolamine (PE) lipids to form phosphatidylcholine (PC) with S-adenosyl-L-[methy-3H]methionine as the methyl donor. Islet PE-N-methyltransferase had activity optima at pH 6-7 and 8-9. S-Adenosyl-L-homocysteine, sodium deoxycholate, and Triton X-100 inhibited methylation in islet homogenates. Addition of phosphatidyl-N-monomethylethanolamine and phosphatidyl-N,N-dimethylethanolamine (PDME) enhanced [3H]methyl incorporation into PDME and PC, respectively. Isoproterenol, but not glucose, stimulated phospholipid methylation in islet homogenates. Propranolol inhibited the isoproterenol effect. In intact islets, glucose or isoproterenol stimulated insulin release and incorporation of [3H]methyl groups from [methyl-3H]methionine into phospholipids. Isoproterenol enhanced to a similar extent glucose-stimulated methylation and hormone release. Neither 2-deoxyglucose, tolbutamide, nor 8-bromo-cyclic AMP stimulated islet phospholipid methylation. The methyl-transferase inhibitor 3-deazaadenosine inhibited both glucose and isoproterenol-stimulated methyltransferase activity and insulin release. Propranolol inhibited the beta-adrenergic potentiation of glucose-induced phospholipid methylation and insulin release. These data suggest that PE-N-methyltransferase plays a role in amplification of the islet cell stimulus-secretion coupling response to certain secretagogues.
大鼠胰岛利用S-腺苷-L-[甲基-³H]甲硫氨酸作为甲基供体，将磷脂酰乙醇胺（PE）脂质甲基化形成磷脂酰胆碱（PC）。胰岛PE-N-甲基转移酶的活性在pH 6 - 7和8 - 9时达到最佳。S-腺苷-L-高半胱氨酸、脱氧胆酸钠和 Triton X - 100抑制胰岛匀浆中的甲基化。添加磷脂酰-N-单甲基乙醇胺和磷脂酰-N,N-二甲基乙醇胺（PDME）分别增强了[³H]甲基掺入PDME和PC。异丙肾上腺素而非葡萄糖刺激胰岛匀浆中的磷脂甲基化。普萘洛尔抑制异丙肾上腺素的作用。在完整胰岛中，葡萄糖或异丙肾上腺素刺激胰岛素释放以及[甲基-³H]甲硫氨酸的[³H]甲基掺入磷脂。异丙肾上腺素在相似程度上增强葡萄糖刺激的甲基化和激素释放。2-脱氧葡萄糖、甲苯磺丁脲和8-溴环磷酸腺苷均未刺激胰岛磷脂甲基化。甲基转移酶抑制剂3-脱氮腺苷抑制葡萄糖和异丙肾上腺素刺激的甲基转移酶活性及胰岛素释放。普萘洛尔抑制β-肾上腺素能对葡萄糖诱导的磷脂甲基化和胰岛素释放的增强作用。这些数据表明PE-N-甲基转移酶在胰岛细胞对某些促分泌剂的刺激-分泌偶联反应的放大中起作用。
