AMPK-mediated increase in myocardial long-chain fatty acid uptake critically depends on sarcolemmal CD36 |
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Authors: | Habets Daphna D J Coumans Will A Voshol Peter J den Boer Marion A M Febbraio Maria Bonen Arend Glatz Jan F C Luiken Joost J F P |
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Institution: | a Department of Molecular Genetics, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands b Department of Endocrinology and Diabetes, Leiden University Medical Center, Leiden, The Netherlands c Departments of Cell Biology and Molecular Cardiology, The Center for Cardiovascular Diagnostics and Prevention, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA d Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ont., Canada N1G 2W1 e Department of Biochemical Physiology and Institute of Biomembranes, Utrecht University, Utrecht, The Netherlands |
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Abstract: | CD36, also named fatty acid translocase, has been identified as a putative membrane transporter for long-chain fatty acids (LCFA). In the heart, contraction-induced 5′ AMP-activated protein kinase (AMPK) signaling regulates cellular LCFA uptake through translocation of CD36 and possibly of other LCFA transporters from intracellular storage compartments to the sarcolemma. In this study, isolated cardiomyocytes from CD36+/+- and CD36−/− mice were used to investigate to what extent basal and AMPK-mediated LCFA uptake are CD36-dependent. Basal LCFA uptake was not altered in CD36−/− cardiomyocytes, most likely resulting from a (1.8-fold) compensatory upregulation of fatty acid-transport protein-1. The stimulatory effect of contraction-mimetic stimuli, oligomycin (2.5-fold) and dipyridamole (1.6-fold), on LCFA uptake into CD36+/+ cardiomyocytes was almost completely lost in CD36−/− cardiomyocytes, despite that AMPK signaling was fully intact. CD36 is almost entirely responsible for AMPK-mediated stimulation of LCFA uptake in cardiomyocytes, indicating a pivotal role for CD36 in mediating changes in cardiac LCFA fluxes. |
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Keywords: | ACC acetyl-CoA carboxylase AICAR d-ribofuranoside" target="_blank">5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside AMPK 5&prime AMP-activated protein kinase CD36 fatty acid translocase CD36 FABPpm plasma membrane fatty acid binding protein FATP fatty acid transport protein GLUT4 glucose transporter 4 LCFA long-chain fatty acids SSP sulfo-N-succinimidylpalmitate |
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