2004
DOI: 10.1007/s00424-003-1199-4
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Regulation of cardiac long-chain fatty acid and glucose uptake by translocation of substrate transporters

Abstract: Cardiac uptake of long-chain fatty acids (FA) is mediated predominantly by two membrane-associated proteins, the 43-kDa plasma membrane fatty acid-binding protein (FABPpm) and the 88-kDa fatty acid translocase/CD36 (FAT/CD36). While FABPpm is present constitutively in the sarcolemma, FAT/CD36 is recycled between an intracellular membrane compartment and the sarcolemma. Since the amount of sarcolemmal FAT/CD36 is a major determinant of cellular FA uptake, understanding of the regulation of its recycling is like… Show more

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Cited by 152 publications
(110 citation statements)
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References 141 publications
(164 reference statements)
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“…Interestingly, incubation of isolated adipocytes with AICAR caused average reductions of 32 and 41% in palmitate and oleate uptake, respectively. Isolated adipocytes reduced by 20,30,40,30, and 40% palmitate and by 42, 55, 41, 41, and 28% oleate uptake after 1-5 min of exposure to these fatty acids, respectively (Fig. 5, A and B).…”
Section: Dose-response Effect Of Compound C On the Production Of 14 Cmentioning
confidence: 92%
“…Interestingly, incubation of isolated adipocytes with AICAR caused average reductions of 32 and 41% in palmitate and oleate uptake, respectively. Isolated adipocytes reduced by 20,30,40,30, and 40% palmitate and by 42, 55, 41, 41, and 28% oleate uptake after 1-5 min of exposure to these fatty acids, respectively (Fig. 5, A and B).…”
Section: Dose-response Effect Of Compound C On the Production Of 14 Cmentioning
confidence: 92%
“…This translocation mechanism for increasing fatty acid uptake by FAT/CD36 resembles the mechanism by which muscle glucose uptake is acutely regulated by redistribution of the glucose transporter GLUT4. The similarity extends even further in that muscle contractions as well as the hormone insulin induce the translocation of both FAT/CD36 and GLUT4 to the muscle cell surface [6]. As a result, modulation of cellular entry appears an important regulatory step not only in glucose metabolism but also in fatty acid metabolism.…”
mentioning
confidence: 82%
“…The exact mechanism for the increased localisation of FAT/CD36 in the sarcolemma is not clear but may relate to the chronic hyperinsulinaemia associated with insulin resistance. It is well established that insulin stimulates FAT/CD36 translocation to the sarcolemma [54,55]. This increased sarcolemmal FAT/CD36 content increases fatty acid uptake in cardiac myocytes and possibly leads to tissue fatty acyl-CoA accumulation if not metabolised through concomitant increased -oxidation [56].…”
Section: The Role Of Free Fatty Acids and Intracellular Lipid Accumulmentioning
confidence: 99%
“…Once inside the cell, non-esterified LCFAs are transported via cytoplasmic heart-type FABPs through the cytoplasm to the location where they will be utilized [193][194][195]. LCFAs are then esterified by acyl-CoA synthetase to form long chain fatty acyl-CoA's (LCFA-CoA) [55]. LCFA-CoAs can be stored in intracellular lipid pools where they can be converted to additional lipid intermediates (triglycerides, diacylglycerol (DAG) or ceramide), or are transported to the mitochondria where they undergo -oxidation.…”
Section: Myocardial Metabolismmentioning
confidence: 99%