Luiken J J, Miskovic D, Arumugam Y, Glatz J F, Bonen A
Department of Physiology, Maastricht University, The Netherlands.
Int J Sport Nutr Exerc Metab. 2001 Dec;11 Suppl:S92-6. doi: 10.1123/ijsnem.11.s1.s92.
While it has long been assumed that long chain fatty acids (LCFA) can freely diffuse across the plasma membrane, recent work has shown that LCFA uptake also involves a protein-mediated mechanism. Three putative LCFA transporters have been identified (FABPpm, FATP, and FAT/CD36), and all are expressed in rodent and human muscles. In a new model system (giant vesicles), we have demonstrated that (a) LCFA transport rates are scaled with the oxidative capacity of heart and muscle, (b) only FABPpm and FAT/CD36, but not FATP1, correlate with vesicular LCFA transport, and (c) LCFA transport can be increased by increasing (1) the FAT/CD36 protein of muscle (chronic adaptation) or (2) via the translocation of FAT/CD36 from an intracellular pool to the plasma membrane during muscle contraction (acute adaptation).
长期以来人们一直认为长链脂肪酸（LCFA）能够自由扩散穿过质膜，但最近的研究表明，LCFA的摄取还涉及一种蛋白质介导的机制。已经鉴定出三种假定的LCFA转运蛋白（FABPpm、FATP和FAT/CD36），它们在啮齿动物和人类肌肉中均有表达。在一个新的模型系统（巨型囊泡）中，我们已经证明：（a）LCFA的转运速率与心脏和肌肉的氧化能力成比例；（b）只有FABPpm和FAT/CD36，而不是FATP1，与囊泡LCFA转运相关；（c）通过增加（1）肌肉中的FAT/CD36蛋白（慢性适应）或（2）在肌肉收缩过程中通过FAT/CD36从细胞内池易位到质膜（急性适应），可以提高LCFA的转运。
