Luiken J J, Glatz J F, Bonen A
Department of Physiology, Maastricht University, Maastricht, The Netherlands.
Can J Appl Physiol. 2000 Oct;25(5):333-52.
In view of the importance of long chain fatty acids (LCFAs) to many cellular processes, it may be desirable to regulate the LCFA disposition in the cell. Such regulation may be present at the level of the plasma membrane, since a number of putative LCFA transport proteins have been cloned. The development of a model system of giant vesicles has proven to be important in identifying the metabolic role of the LCFA transport system. LCFA transport rates and transporters (FABPpm and FAT/CD36) are scaled with oxidative capacity of heart and muscle. FAT/CD36 is a critical LCFA transport protein in muscle. With chronic contraction the increase in this protein also results in an increase in LCFA transport. Most importantly, LCFA transport is also increased acutely by muscle contraction, involving the translocation of FAT/CD36 from intracellular depots to the surface of the muscle cell. The acute (minutes) and chronic (days) regulation of LCFA transporters and transport by muscle may be an important mechanism for LCFA utilization during exercise and adaptable with training and with a metabolic disease such as type 2 diabetes.
鉴于长链脂肪酸（LCFAs）对许多细胞过程的重要性，调节细胞内LCFAs的处置可能是必要的。由于已经克隆了许多假定的LCFA转运蛋白，这种调节可能存在于质膜水平。巨囊泡模型系统的开发已被证明在确定LCFA转运系统的代谢作用方面很重要。LCFA转运速率和转运蛋白（FABPpm和FAT/CD36）与心脏和肌肉的氧化能力成比例。FAT/CD36是肌肉中一种关键的LCFA转运蛋白。随着慢性收缩，这种蛋白质的增加也会导致LCFA转运增加。最重要的是，肌肉收缩也会急性增加LCFA转运，这涉及FAT/CD36从细胞内储存库转运到肌肉细胞表面。肌肉对LCFA转运蛋白和转运的急性（分钟）和慢性（天）调节可能是运动期间LCFA利用的重要机制，并且可随着训练以及患有2型糖尿病等代谢疾病而发生适应性变化。
