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This Article Full Text Full Text (PDF) All Versions of this Article: 573/1/199    most recent jphysiol.2006.106013v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Benton, C. R. Articles by Bonen, A. Search for Related Content PubMed PubMed Citation Articles by Benton, C. R. Articles by Bonen, A. Related Collections Integrative

¹ Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1
² Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1
³ Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, the Netherlands
⁴ Section of Endocrinology and Metabolism, Wake Forest University School of Medicine and Baptist Medical Center, Winston-Salem, NC 27157, USA
⁵ Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories, 9900 Medical Center Drive, Rockville, MD 20850, USA
⁶ Department of Biochemical Physiology and Institute of Biomembranes, Utrecht University, Utrecht, the Netherlands
⁷ Department of Biology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1

We have examined over the course of a 1-week period the independent and combined effects of chronically increased muscle contraction and the peroxisome proliferator-activated receptor (PPAR) and PPAR activators, Wy 14,643 and rosiglitazone, on the expression and plasmalemmal content of the fatty acid transporters, FAT/CD36 and FABPpm, as well as on the rate of fatty acid transport. In resting muscle, the activation of either PPAR or PPAR failed to induce the protein expression of FAT/CD36. PPAR activation also failed to induce the protein expression of FABPpm. In contrast, PPAR activation induced the expression of FABPpm protein (40%; P < 0.05). Chronic muscle contraction increased the protein expression of FAT/CD36 (50%; P < 0.05), whereas FABPpm was slightly increased (12%; P < 0.05). Neither PPAR nor PPAR activation altered the contraction-induced expression of FAT/CD36 or FABPpm. Changes in protein expression of FAT/CD36 or FABPpm, induced by either contractions or by administration of rosiglitazone, were largely attributable to increased transcription. The contraction-induced increments in FAT/CD36 were accompanied by parallel increments in plasmalemmal FAT/CD36 and in rates of fatty acid transport (P < 0.05). Up-regulation of FABPpm expression was, however, accompanied by a reduction in plasmalemmal FABPpm, which did not affect the rates of long chain fatty acid (LCFA) transport. These studies have shown that in skeletal muscle (i) neither PPAR nor PPAR activation alters FAT/CD36 expression, (ii) PPAR activation selectively up-regulates FABPpm expression and (iii) contraction-induced up-regulation of LCFA transport does not appear to occur via activation of either PPAR or PPAR.

(Received 23 January 2006; accepted after revision 14 February 2006; first published online 16 February 2006)
Corresponding author A. Bonen: Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1. Email: abonen{at}uoguelph.ca

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