Phosphatidylethanolamine methyltransferase activity in developing, demyelinating, and diabetic mouse brain.
Phosphatidylethanolamine methyltransferase activity in developing, demyelinating, and diabetic mouse brain.
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发育中、脱髓鞘和糖尿病小鼠大脑中磷脂酰乙醇胺甲基转移酶的活性。
DOI：
10.1620/tjem.141.suppl_485
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Yoshiharu Akazawa
中科院分区：
文献类型：
--
作者：
Shin;Kazuhiko Sudou;Aya Imoh;M. Koide;Yoshiharu Akazawa
在髓鞘形成活跃的小鼠脑中，以S-腺苷甲硫氨酸为甲基供体，磷脂酰乙醇胺甲基转移酶（PEMT）催化磷脂酰胆碱（PC）的合成。孕17天的胎鼠脑微粒体部分的PEMT活性为253 μ u/mg蛋白质，6周的铜腙给药后髓鞘再生7天的成年脑微粒体部分的PEMT活性为148 μ u/mg。这些数字远高于正常成人大脑中发现的（1.7 μ u/mg）。在遗传性糖尿病小鼠（C57 BL/KsJ-db/db）和链脲佐菌素诱导的糖尿病小鼠的脑中观察到PEMT活性增加，分别为16.3和9.2 μ u/mg。甲钴胺的甲基被转移到产生同型半胱氨酸的蛋氨酸，并在脑片中进一步代谢为胆碱和乙酰胆碱。这些结果表明，在糖尿病状态下，PC合成的增加可能是必需的，以取代受损的髓鞘或供应胆碱或乙酰胆碱对神经功能至关重要。甲钴胺可能作为来源的甲基用于PC的合成。
The catalysis by phosphatidylethanolamine methyltransferase (PEMT) of phosphatidylcholine (PC) synthesis by the successive methylation of phosphatidylethanolamine in the presence of S-adenosylmethionine (AdoMet) as methyl donor, was detected in actively myelinating mouse brains. PEMT activity in the microsome fraction of fetal mouse brain at 17 days of gestation was 253 mu u/mg protein and that of adult brain after 7 days of remyelination following 6 weeks cuprizone administration was 148 mu u/mg. These figures are much higher than found in normal adult brains (1.7 mu u/mg). An increase in PEMT activity was observed in the brains of genetically transmitted diabetic mice, C57BL/KsJ-db/db, and streptozotocin-induced diabetic mice; 16.3 and 9.2 mu u/mg, respectively. The methyl group of mecobalamin was transferred to homocysteine producing AdoMet and was further metabolized into choline and acetylcholine in brain slices. These results suggest that in the diabetic state, an increase in PC synthesis is probably required in order to replace damaged myelin or to supply choline or acetylcholine essential to for nerve functions. Mecobalamin might serve as the source of the methyl group utilized for PC synthesis.