| Caffeine-stimulated fatty acid oxidation is blunted in CD36 null mice. | |
| | |
MedLine Citation:
|
PMID: 22463611 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
|
AIM: The increase in skeletal muscle fatty acid metabolism during exercise has been associated with the release of calcium. We examined whether this increase in fatty acid oxidation was attributable to a calcium-induced translocation of the fatty acid transporter CD36 to the sarcolemma, thereby providing an enhanced influx of fatty acids to increase their oxidation. METHODS: Calcium release was triggered by caffeine (3 mm) to examine fatty acid oxidation in intact soleus muscles of WT and CD36-KO mice, while fatty acid transport and mitochondrial fatty acid oxidation were examined in giant vesicles and isolated mitochondria, respectively, from caffeine-perfused hindlimb muscles of WT and CD36-KO mice. Western blotting was used to examine calcium-induced signalling. RESULTS: In WT, caffeine stimulated muscle palmitate oxidation (+136%), but this was blunted in CD36-KO mice (-70%). Dantrolene inhibited (WT) or abolished (CD36-KO) caffeine-induced palmitate oxidation. In muscle, caffeine-stimulated palmitate oxidation was not attributable to altered mitochondrial palmitate oxidation. Instead, in WT, caffeine increased palmitate transport (+55%) and the translocation of fatty acid transporters CD36, FABPpm, FATP1 and FATP4 (26-70%) to the sarcolemma. In CD36-KO mice, caffeine-stimulated FABPpm, and FATP1 and 4 translocations were normal, but palmitate transport was blunted (-70%), comparable to the reductions in muscle palmitate oxidation. Caffeine did not alter the calcium-/calmodulin-dependent protein kinase II phosphorylation but did increase the phosphorylation of AMPK and acetyl-CoA carboxylase comparably in WT and CD36-KO. CONCLUSION: These studies indicate that sarcolemmal CD36-mediated fatty acid transport is a primary mediator of the calcium-induced increase in muscle fatty acid oxidation. |
| | |
Authors:
|
J S V Lally; S S Jain; X X Han; L A Snook; J F C Glatz; J J F P Luiken; J McFarlan; G P Holloway; A Bonen |
Publication Detail:
|
Type: Journal Article |
Journal Detail:
|
Title: Acta physiologica (Oxford, England) Volume: 205 ISSN: 1748-1716 ISO Abbreviation: Acta Physiol (Oxf) Publication Date: 2012 May |
Date Detail:
|
Created Date: 2012-04-02 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101262545 Medline TA: Acta Physiol (Oxf) Country: England |
Other Details:
|
Languages: eng Pagination: 71-81 Citation Subset: IM |
Copyright Information:
|
© 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society. |
Affiliation:
|
Department of Human Health and Nutritional Science, University of Guelph, Guelph, ON, Canada. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: CB(1) receptor antagonists: new discoveries leading to new perspectives.
Next Document: Chronic endothelin A receptor blockade attenuates contribution of sympathetic nervous system to salt...