Sarcolemmal fatty acid transport in normal and diseased hearts.

Our knowledge about the regulation of myocardial fatty acid uptake has increased dramatically in the past decade. Fatty acid uptake was found to occur by a mechanism resembling that of cellular glucose uptake. Thus, 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, just like these same stimuli recruit glucose transporters to increase glucose uptake. Studies in humans and in animal models have implicated dysregulation of fatty acid transporters in disease pathogenesis, such as the progression of obesity to insulin resistance and diabetic cardiomyopathy. As a result, membrane fatty acid transporters are now regarded as a promising therapeutic target to rectify abnormalities in cardiac fatty acid use in chronic cardiac disease.