| In vivo, fatty acid translocase (CD36) critically regulates skeletal muscle fuel selection, exercise performance, and training-induced adaptation of fatty acid oxidation. | |
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MedLine Citation:
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PMID: 22584574 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2012-05-14 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 287 ISSN: 1083-351X ISO Abbreviation: J. Biol. Chem. Publication Date: 2012 Jul |
Date Detail:
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Created Date: 2012-07-09 Completed Date: 2012-10-09 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 23502-16 Citation Subset: IM |
Affiliation:
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Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological
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genetics,
physiology* Animals Antigens, CD36 / deficiency, genetics, metabolism* Biological Transport Blotting, Western Fatty Acids / metabolism* Glucose / metabolism Liver Glycogen / metabolism Mice Mice, Knockout Mitochondria, Muscle / metabolism Muscle, Skeletal / metabolism* Oxidation-Reduction Oxygen Consumption Physical Conditioning, Animal / physiology* Sarcolemma / metabolism Triglycerides / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD36; 0/Fatty Acids; 0/Liver Glycogen; 0/Triglycerides; 50-99-7/Glucose |
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