Prolonged AMPK Activation Increases the Expression of Fatty Acid Transporters in Cardiac Myocytes and Perfused Hearts (Q27887311)

Adrian Chabowski

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Joost J F P Luiken

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Joost J. F. P. Luiken

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Arend Bonen

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Arend Bonen

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Jan F.C. Glatz

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Jan F. C. Glatz

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author name string

Iman Momken

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Jorge Calles-Escandon

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Narendra N. Tandon

Molecular and Cellular Biochemistry

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publication date

19 May 2006

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number of pages

12

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published in

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https://scigraph.springernature.com/pub.10.1007/s11010-006-9140-8

volume

288

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issue

1-2

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page(s)

201-212

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exact match

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cites work

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AMPK stimulation increases LCFA but not glucose clearance in cardiac muscle in vivo

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The membrane-associated 40 KD fatty acid binding protein (Berk's protein), a putative fatty acid transporter is present in human skeletal muscle

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Highly insulin-responsive isolated rat heart muscle cells yielded by a modified isolation method

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The subcellular compartmentation of fatty acid transporters is regulated differently by insulin and by AICAR

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Translocation of myocardial GLUT-4 and increased glucose uptake through activation of AMPK by AICAR.

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High rates of fatty acid oxidation during reperfusion of ischemic hearts are associated with a decrease in malonyl-CoA levels due to an increase in 5'-AMP-activated protein kinase inhibition of acetyl-CoA carboxylase

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Leptin activates cardiac fatty acid oxidation independent of changes in the AMP-activated protein kinase-acetyl-CoA carboxylase-malonyl-CoA axis

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Insulin stimulates long-chain fatty acid utilization by rat cardiac myocytes through cellular redistribution of FAT/CD36.

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Acute regulation of fatty acid uptake involves the cellular redistribution of fatty acid translocase

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AMP kinase activation with AICAR simultaneously increases fatty acid and glucose oxidation in resting rat soleus muscle

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Dipyridamole alters cardiac substrate preference by inducing translocation of FAT/CD36, but not that of GLUT4.

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Insulin stimulates fatty acid transport by regulating expression of FAT/CD36 but not FABPpm

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