Electrostimulation enhances FAT/CD36-mediated long-chain fatty acid uptakeby isolated rat cardiac myocytes

We investigated palmitate uptake and utilization by contracting cardiac myo cytes in suspension to explore the link between long-chain fatty acid (FA) uptake and cellular metabolism, in particular the role of fatty acid transl ocase (FAT)/CD36-mediated transsarcolemmal FA transport. For this, an exper imental setup was developed to electrically stimulate cardiomyocytes in mul tiple parallel incubations. Electrostimulation at voltages greater than or equal to 170 V resulted in, cellular contraction with no detrimental effect on cellular integrity. At 200 V and 4 Hz, palmitate uptake (measured after 3-min incubation) was enhanced 1.5-fold. In both quiescent and contracting myocytes, after their uptake, palmitate was largely and rapidly esterified , mainly into triacylglycerols. Palmitate oxidation (measured after 30 min) contributed to 22% of palmitate taken up by quiescent cardiomyocytes and, after stimulation at 4 Hz, was increased 2.8-fold to contribute to 39% of p almitate utilization. The electrostimulation-mediated increase in palmitate uptake was blocked in the presence of either verapamil, a contraction inhi bitor, or sulfo-N-succinimidyl-FA esters, specific inhibitors of FAT/CD36. These data indicate that, in contracting cardiac myocytes, palmitate uptake is increased due to, increased flux through FAT/CD36.