AMPK-mediated increase in myocardial long-chain fatty acid uptake critically depends on sarcolemmal CD36

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 LCF...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-03, Vol.355 (1), p.204-210
Main 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.
Format: Article
Language:English
Subjects:
5′ AMP-activated protein kinase
Adenylate Kinase - metabolism
Animals
Biological Transport
CD36
CD36 Antigens - genetics
CD36 Antigens - physiology
Deoxyglucose - metabolism
Dipyridamole
Fatty acid binding proteins
Fatty acid uptake
Fatty Acids, Nonesterified - metabolism
Heart - drug effects
Heart - physiology
Kinetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Contraction - drug effects
Myocardium - enzymology
Myocardium - metabolism
Oligomycin
Oligomycins - pharmacology
Palmitic Acid - metabolism
Sarcolemma - metabolism
Sulfo- N-succinimidylpalmitate
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2007.01.141