Document Detail

In vivo, fatty acid translocase (CD36) critically regulates skeletal muscle fuel selection, exercise performance, and training-induced adaptation of fatty acid oxidation.
MedLine Citation:
PMID:  22584574     Owner:  NLM     Status:  MEDLINE    
For ~40 years it has been widely accepted that (i) the exercise-induced increase in muscle fatty acid oxidation (FAO) is dependent on the increased delivery of circulating fatty acids, and (ii) exercise training-induced FAO up-regulation is largely attributable to muscle mitochondrial biogenesis. These long standing concepts were developed prior to the recent recognition that fatty acid entry into muscle occurs via a regulatable sarcolemmal CD36-mediated mechanism. We examined the role of CD36 in muscle fuel selection under basal conditions, during a metabolic challenge (exercise), and after exercise training. We also investigated whether CD36 overexpression, independent of mitochondrial changes, mimicked exercise training-induced FAO up-regulation. Under basal conditions CD36-KO versus WT mice displayed reduced fatty acid transport (-21%) and oxidation (-25%), intramuscular lipids (less than or equal to -31%), and hepatic glycogen (-20%); but muscle glycogen, VO(2max), and mitochondrial content and enzymes did not differ. In acutely exercised (78% VO(2max)) CD36-KO mice, fatty acid transport (-41%), oxidation (-37%), and exercise duration (-44%) were reduced, whereas muscle and hepatic glycogen depletions were accelerated by 27-55%, revealing 2-fold greater carbohydrate use. Exercise training increased mtDNA and β-hydroxyacyl-CoA dehydrogenase similarly in WT and CD36-KO muscles, but FAO was increased only in WT muscle (+90%). Comparable CD36 increases, induced by exercise training (+44%) or by CD36 overexpression (+41%), increased FAO similarly (84-90%), either when mitochondrial biogenesis and FAO enzymes were up-regulated (exercise training) or when these were unaltered (CD36 overexpression). Thus, sarcolemmal CD36 has a key role in muscle fuel selection, exercise performance, and training-induced muscle FAO adaptation, challenging long held views of mechanisms involved in acute and adaptive regulation of muscle FAO.
Jay T McFarlan; Yuko Yoshida; Swati S Jain; Xioa-Xia Han; Laelie A Snook; James Lally; Brennan K Smith; Jan F C Glatz; Joost J F P Luiken; Ryan A Sayer; A Russell Tupling; Adrian Chabowski; Graham P Holloway; Arend Bonen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-05-14
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  287     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-07-09     Completed Date:  2012-10-09     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  23502-16     Citation Subset:  IM    
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada.
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MeSH Terms
Adaptation, Physiological / genetics,  physiology*
Antigens, CD36 / deficiency,  genetics,  metabolism*
Biological Transport
Blotting, Western
Fatty Acids / metabolism*
Glucose / metabolism
Liver Glycogen / metabolism
Mice, Knockout
Mitochondria, Muscle / metabolism
Muscle, Skeletal / metabolism*
Oxygen Consumption
Physical Conditioning, Animal / physiology*
Sarcolemma / metabolism
Triglycerides / metabolism
Grant Support
//Canadian Institutes of Health Research
Reg. No./Substance:
0/Antigens, CD36; 0/Fatty Acids; 0/Liver Glycogen; 0/Triglycerides; 50-99-7/Glucose

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