Authors: Benton, Carley R.; Koonen, Debby P. Y.¹; Calles-Escandon, Jorge²; Tandon, Narendra N.³; Glatz, Jan F. C.¹; Luiken, Joost J. F. P.; Heikkila, John J.⁴; Bonen, Arend⁵

Source: The Journal of Physiology, Volume 573, Number 1, May 2006 , pp. 199-210(12)

Publisher: Wiley-Blackwell

Abstract:

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)α and PPARγ 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 PPARα or PPARγ failed to induce the protein expression of FAT/CD36. PPARα activation also failed to induce the protein expression of FABPpm. In contrast, PPARγ 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 PPARα nor PPARγ 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 PPARα nor PPARγ activation alters FAT/CD36 expression, (ii) PPARγ activation selectively up-regulates FABPpm expression and (iii) contraction-induced up-regulation of LCFA transport does not appear to occur via activation of either PPARα or PPARγ.

Document Type: Research article

DOI: http://dx.doi.org/10.1113/jphysiol.2006.106013

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

Publication date: 2006-05-01

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