Joost J. F. P. Luiken

TL;DR: In this article, it was shown that following an acute stimulus, particularly insulin or muscle contraction, specific fatty acid transporters translocate from intracellular stores to the plasma membrane to facilitate fatty acid uptake.

TL;DR: FAT/CD36 provides another potential therapeutic target for the prevention and/or treatment of insulin resistance and the increased rate of fatty acid transport may contribute to the increased rates of triacylglycerol accumulation in human skeletal muscle.

TL;DR: It is concluded that AMP kinase regulates cardiac FA use through mobilization of FAT/CD36 from a contraction-inducible intracellular storage compartment.

TL;DR: A role for FAT/CD36 in mitochondrial long chain fatty acid uptake is suggested and system flexibility is demonstrated to match FAT/ CD36 mitochondrial content with an increased capacity for fatty acid oxidation, possibly involving translocation of FAT/cd36 to the mitochondria.

TL;DR: A novel role of insulin in cardiac FA utilization is demonstrated and Malfunctioning of insulin-induced FAT/CD36 translocation may be involved in the development of type 2 diabetic cardiomyopathies.