Document Detail

Fatty acid translocase/CD36 deficiency does not energetically or functionally compromise hearts before or after ischemia.
MedLine Citation:
PMID:  15023869     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Evidence from humans suggests that fatty acid translocase (FAT)/CD36 deficiency can lead to functionally and/or energetically compromised hearts, but the data are equivocal, and the subject remains controversial. In this report we assessed the contribution of FAT/CD36 to overall fatty acid oxidation rates in the intact heart and determined the effect of FAT/CD36 on energy metabolism during reperfusion of ischemic hearts. METHODS AND RESULTS: Isolated working hearts from wild-type and FAT/CD36-knockout (KO) mice were perfused with Krebs-Henseleit solution containing 0.4 or 1.2 mmol/L [U-3H]palmitate, 5 mmol/L [U-14C]glucose, 2.5 mmol/L calcium, and 100 microU/mL insulin at a preload pressure of 11.5 mm Hg and afterload pressure of 50 mm Hg. Hearts were aerobically perfused for 30 minutes or aerobically perfused for 30 minutes, followed by 18 minutes of global no-flow ischemia and 40 minutes of aerobic reperfusion. Rates of fatty acid oxidation in FAT/CD36-KO hearts were significantly lower than in wild-type hearts at both concentrations of palmitate (0.4 or 1.2 mmol/L). In addition, hearts from FAT/CD36-KO mice displayed a compensatory increase in glucose oxidation rates. On aerobic reperfusion after ischemia, cardiac work of FAT/CD36-KO hearts recovered to the same extent as wild-type hearts. CONCLUSIONS: FAT/CD36-deficient hearts are not energetically or functionally compromised and are not more sensitive to ischemic injury because glucose oxidation can compensate for the loss of fatty acid-derived ATP.
Michael Kuang; Maria Febbraio; Cory Wagg; Gary D Lopaschuk; Jason R B Dyck
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-03-15
Journal Detail:
Title:  Circulation     Volume:  109     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-03-30     Completed Date:  2004-07-15     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1550-7     Citation Subset:  AIM; IM    
Cardiovascular Research Group, Department of Pediatrics, Faculty of Medicine, University of Alberta, Edmonton, Alberta, Canada.
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MeSH Terms
Adenosine Triphosphate / metabolism
Antigens, CD36 / genetics,  physiology
Energy Metabolism*
Fatty Acids / metabolism
Glucose / metabolism
Mice, Inbred C57BL
Mice, Knockout
Myocardial Ischemia / metabolism*
Myocardium / metabolism*
Organic Anion Transporters / deficiency*,  genetics,  physiology
Palmitates / metabolism
Reg. No./Substance:
0/Antigens, CD36; 0/Fatty Acids; 0/Organic Anion Transporters; 0/Palmitates; 50-99-7/Glucose; 56-65-5/Adenosine Triphosphate

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

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