Insulin Stimulates Long-Chain Fatty Acid Utilization by Rat Cardiac Myocytes Through Cellular Redistribution of FAT/CD36

• DOI: 10.2337/diabetes.51.10.3113
• Publication Date: 2007-03-06T19:04:22Z
• Authors: Joost J.F.P. Luiken; Debby P.Y. Koonen; Jodil Willems; Antonio Zorzano; Christoph Becker; Yvan Fischer; Narendra N. Tandon; Ger J. van der Vusse; Arend Bonen; Jan F.C. Glatz
• Keywords: CD36; GLUT4; Wortmannin

The existence of an intracellular pool fatty acid translocase (FAT/CD36), 88-kDa membrane transporter for long-chain acids (FAs), and the ability insulin to induce translocation events prompted us investigate direct effects on cellular uptake FA by heart. Insulin (0.1 nmol/l higher) increased isolated rat cardiac myocytes 1.5-fold. This insulin-induced increase in was completely blocked phloretin, sulfo-N-succinimidylpalmitate (SSP), wortmannin, indicating involvement FAT/CD36 dependence phosphatidylinositol-3 (PI-3) kinase activation. Subcellular fractionation insulin-stimulated demonstrated a 1.5-fold sarcolemmal 62% decrease with parallel changes subcellular distribution GLUT4. Induction contractions upon electrostimulation at 4 Hz enhanced 1.6-fold, independent PI-3 kinase. addition Hz-stimulated cells further stimulated 2.3-fold, that there are least two functionally pools, one recruited other mobilized contractions. In conclusion, we have novel role utilization. Malfunctioning may be involved development type 2 diabetic cardiomyopathies.