Long-chain fatty acid uptake and FAT/CD36 translocation in heart and skeletal muscle

被引:200
作者
Koonen, DPY
Glatz, JFC
Bonen, A
Luiken, JJFP [1 ]
机构
[1] Maastricht Univ, Cardiovasc Res Inst Maastricht, Dept Mol Genet, NL-6200 MD Maastricht, Netherlands
[2] Univ Guelph, Dept Human Biol & Nutr Sci, Guelph, ON N1G 2W1, Canada
[3] Univ Utrecht, Dept Biochem Physiol, Utrecht, Netherlands
[4] Univ Utrecht, Biomembrane Inst, Utrecht, Netherlands
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS | 2005年 / 1736卷 / 03期
基金
加拿大自然科学与工程研究理事会; 加拿大健康研究院;
关键词
long-chain fatty acid uptake; FAT/CD36; insulin; PI(3)K; contraction; GLUT4;
D O I
10.1016/j.bbalip.2005.08.018
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cellular long-chain fatty acid (LCFA) uptake constitutes a process that is not yet fully understood. LCFA uptake likely involves both passive diffusion and protein-mediated transport. Several lines of evidence support the involvement of a number of plasma membrane-associated proteins, including fatty acid translocase (FAT)/CD36, plasma membrane-bound fatty acid binding protein (FABPpm), and fatty acid transport protein (FATP). In heart and skeletal muscle primary attention has been given to unravel the mechanisms by which FAT/CD36 expression and function are regulated. It appears that both insulin and contractions induce the translocation of intracellular stored FAT/CD36 to the plasma membrane to increase cellular LCFA uptake. This review focuses on this novel mechanism of regulation of LCFA uptake in heart and skeletal muscle in health and disease. The distinct signaling pathways underlying insulin-induced and contraction-induced FAT/CD36 translocation will be discussed and a comparison will be made with the well-defined glucose transport system involving the glucose transporter GLUT4. Finally, it is hypothesized that malfunctioning of recycling of these transporters may lead to intracellular triacylglycerol (TAG) accumulation and cellular insulin resistance. Current data indicate a pivotal role for FAT/CD36 in the regulation of LCFA utilization in heart and skeletal muscle under normal conditions as well as during the altered LCFA utilization observed in obesity and insulin resistance. Hence, FAT/CD36 might provide a useful therapeutic target for the prevention or treatment of insulin resistance. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:163 / 180
页数:18
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