Document Detail


Prolonged AMPK activation increases the expression of fatty acid transporters in cardiac myocytes and perfused hearts.
MedLine Citation:
PMID:  16710744     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recently, fatty acid transport across the plasma membrane has been shown to be a key process that contributes to the regulation of fatty acid metabolism in the heart. Since AMP kinase activation by 5-aminoimidazole-4-carboxamide-1-beta-D: -ribofuranoside (AICAR) stimulates fatty acid oxidation, as well as the expression of selected proteins involved with energy provision, we examined (a) whether AICAR induced the expression of the fatty acid transporters FABPpm and FAT/CD36 in cardiac myocytes and in perfused hearts and (b) the signaling pathway involved. Incubation of cardiac myocytes with AICAR increased the protein expression of the fatty acid transporter FABPpm after 90 min (+27%, P < 0.05) and this protein remained stably overexpressed until 180 min. Similarly, FAT/CD36 protein expression was increased after 60 min (+38%, P < 0.05) and remained overexpressed thereafter. Protein overexpression, which occurred via transcriptional mechanisms, was dependent on the AICAR concentration, with optimal induction occurring at AICAR concentrations 1-5 mM for FABPpm and at 2-8 mM for FAT/CD36. The AICAR (2 h, 2 mM AICAR) effects on FABPpm and FAT/CD36 protein expression were similar in perfused hearts and in cardiac myocytes. AICAR also induced the plasmalemmal content of FAT/CD36 (+49%) and FABPpm (+42%) (P < 0.05). This was accompanied by a marked increase in the rate of palmitate transport (2.5 fold) into giant sarcolemmal vesicles, as well as by increased rates of palmitate oxidation in cardiac myocytes. When the AICAR-induced AMPK phosphorylation was blocked, neither FAT/CD36 nor FABPpm were overexpressed, nor were palmitate uptake and oxidation increased. This study has revealed that AMPK activation stimulates the protein expression of both fatty acid transporters, FAT/CD36 and FABPpm in (a) time- and (b) dose-dependent manner via (c) the AMPK signaling pathway. AICAR also (d) increased the plasmalemmal content of FAT/CD36 and FABPm, thereby (e) increasing the rates of fatty acid transport. Thus, activation of AMPK is a key mechanism regulating the expression as well as the plasmalemmal localization of fatty acid transporters.
Authors:
Adrian Chabowski; Iman Momken; Susan L M Coort; Jorge Calles-Escandon; Narendra N Tandon; Jan F C Glatz; Joost J F P Luiken; Arend Bonen
Related Documents :
12479584 - Regulation of fatty acid transport and membrane transporters in health and disease.
5259774 - Na plus-facilitated reactions of neutral amino acids with a cationic amino acid transpo...
16126914 - Serotonin, l-tryptophan, and tryptamine are effective inhibitors of the amino acid tran...
7060564 - Picrate as an inhibitor of photosystem ii in photosynthetic electron transport.
746344 - Phosphatidylcholine substrate specificity of lecithin:cholesterol acyltransferase.
27224 - Excitation of indole-3-acetic acid (an auxin) in a linoleate-lipoxygenase system.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-05-19
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  288     ISSN:  0300-8177     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-08-31     Completed Date:  2007-01-10     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  201-12     Citation Subset:  IM    
Affiliation:
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, N1G 2W1, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases
Aminoimidazole Carboxamide / analogs & derivatives,  pharmacology
Animals
Antigens, CD36 / metabolism*
Dose-Response Relationship, Drug
Fatty Acid-Binding Proteins / metabolism*
Fatty Acids / metabolism
Hypoglycemic Agents / pharmacology
Male
Multienzyme Complexes / metabolism*
Myocardium / enzymology,  metabolism*
Myocytes, Cardiac / drug effects,  enzymology,  metabolism*
Oxidation-Reduction
Protein-Serine-Threonine Kinases / metabolism*
Rats
Rats, Wistar
Ribonucleotides / pharmacology
Signal Transduction
Chemical
Reg. No./Substance:
0/Antigens, CD36; 0/FABPpm protein, rat; 0/Fatty Acid-Binding Proteins; 0/Fatty Acids; 0/Hypoglycemic Agents; 0/Multienzyme Complexes; 0/Ribonucleotides; 3031-94-5/AICA ribonucleotide; 360-97-4/Aminoimidazole Carboxamide; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Effects of various oxidants and antioxidants on the p38-MAPK signalling pathway in the perfused amph...
Next Document:  Activity of lysosomal exoglycosidases in human gliomas.