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Rosiglitazone increases fatty acid oxidation and fatty acid translocase (FAT/CD36) but not carnitine palmitoyltransferase I in rat muscle mitochondria.
J Physiol. 2008 Mar 15; 586(6):1755-66.JP

Abstract

Peroxisome proliferator-activated receptors (PPARs) alter the expression of genes involved in regulating lipid metabolism. Rosiglitazone, a PPARgamma agonist, induces tissue-specific effects on lipid metabolism; however, its mode of action in skeletal muscle remains unclear. Since fatty acid translocase (FAT/CD36) was recently identified as a possible regulator of skeletal muscle fatty acid transport and mitochondrial fatty acid oxidation, we examined in this tissue the effects of rosiglitazone infusion (7 days, 1 mg day(-1)) on FAT/CD36 mRNA and protein, its plasmalemmal content and fatty acid transport. In addition, in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria we examined rates of fatty acid oxidation, FAT/CD36 and carnitine palmitoyltransferase I (CPTI) protein, and CPTI and beta-hydroxyacyl CoA dehydrogenase (beta-HAD) activities. Rosiglitazone did not alter FAT/CD36 mRNA or protein expression, FAT/CD36 plasmalemmal content, or the rate of fatty acid transport into muscle (P > 0.05). In contrast, rosiglitazone increased the rates of fatty acid oxidation in both SS (+21%) and IMF mitochondria (+36%). This was accompanied by concomitant increases in FAT/CD36 in subsarcolemmal (SS) (+43%) and intermyofibrillar (IMF) mitochondria (+46%), while SS and IMF CPTI protein content, and CPTI submaximal and maximal activities (P > 0.05) were not altered. Similarly, citrate synthase (CS) and beta-HAD activities were also not altered by rosiglitazone in SS and IMF mitochondria (P > 0.05). These studies provide another example whereby changes in mitochondrial fatty oxidation are associated with concomitant changes in mitochondrial FAT/CD36 independent of any changes in CPTI. Moreover, these studies identify for the first time a mechanism by which rosiglitazone stimulates fatty acid oxidation in skeletal muscle, namely the chronic, subcellular relocation of FAT/CD36 to mitochondria.

Authors+Show Affiliations

Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada. abonen@uoguelph.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18238811

Citation

Benton, Carley R., et al. "Rosiglitazone Increases Fatty Acid Oxidation and Fatty Acid Translocase (FAT/CD36) but Not Carnitine Palmitoyltransferase I in Rat Muscle Mitochondria." The Journal of Physiology, vol. 586, no. 6, 2008, pp. 1755-66.
Benton CR, Holloway GP, Campbell SE, et al. Rosiglitazone increases fatty acid oxidation and fatty acid translocase (FAT/CD36) but not carnitine palmitoyltransferase I in rat muscle mitochondria. J Physiol (Lond). 2008;586(6):1755-66.
Benton, C. R., Holloway, G. P., Campbell, S. E., Yoshida, Y., Tandon, N. N., Glatz, J. F., Luiken, J. J., Spriet, L. L., & Bonen, A. (2008). Rosiglitazone increases fatty acid oxidation and fatty acid translocase (FAT/CD36) but not carnitine palmitoyltransferase I in rat muscle mitochondria. The Journal of Physiology, 586(6), 1755-66. https://doi.org/10.1113/jphysiol.2007.146563
Benton CR, et al. Rosiglitazone Increases Fatty Acid Oxidation and Fatty Acid Translocase (FAT/CD36) but Not Carnitine Palmitoyltransferase I in Rat Muscle Mitochondria. J Physiol (Lond). 2008 Mar 15;586(6):1755-66. PubMed PMID: 18238811.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosiglitazone increases fatty acid oxidation and fatty acid translocase (FAT/CD36) but not carnitine palmitoyltransferase I in rat muscle mitochondria. AU - Benton,Carley R, AU - Holloway,Graham P, AU - Campbell,S E, AU - Yoshida,Yuko, AU - Tandon,Narendra N, AU - Glatz,Jan F C, AU - Luiken,Joost J J F P, AU - Spriet,Lawrence L, AU - Bonen,Arend, Y1 - 2008/01/31/ PY - 2008/2/2/pubmed PY - 2008/4/24/medline PY - 2008/2/2/entrez SP - 1755 EP - 66 JF - The Journal of physiology JO - J. Physiol. (Lond.) VL - 586 IS - 6 N2 - Peroxisome proliferator-activated receptors (PPARs) alter the expression of genes involved in regulating lipid metabolism. Rosiglitazone, a PPARgamma agonist, induces tissue-specific effects on lipid metabolism; however, its mode of action in skeletal muscle remains unclear. Since fatty acid translocase (FAT/CD36) was recently identified as a possible regulator of skeletal muscle fatty acid transport and mitochondrial fatty acid oxidation, we examined in this tissue the effects of rosiglitazone infusion (7 days, 1 mg day(-1)) on FAT/CD36 mRNA and protein, its plasmalemmal content and fatty acid transport. In addition, in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria we examined rates of fatty acid oxidation, FAT/CD36 and carnitine palmitoyltransferase I (CPTI) protein, and CPTI and beta-hydroxyacyl CoA dehydrogenase (beta-HAD) activities. Rosiglitazone did not alter FAT/CD36 mRNA or protein expression, FAT/CD36 plasmalemmal content, or the rate of fatty acid transport into muscle (P > 0.05). In contrast, rosiglitazone increased the rates of fatty acid oxidation in both SS (+21%) and IMF mitochondria (+36%). This was accompanied by concomitant increases in FAT/CD36 in subsarcolemmal (SS) (+43%) and intermyofibrillar (IMF) mitochondria (+46%), while SS and IMF CPTI protein content, and CPTI submaximal and maximal activities (P > 0.05) were not altered. Similarly, citrate synthase (CS) and beta-HAD activities were also not altered by rosiglitazone in SS and IMF mitochondria (P > 0.05). These studies provide another example whereby changes in mitochondrial fatty oxidation are associated with concomitant changes in mitochondrial FAT/CD36 independent of any changes in CPTI. Moreover, these studies identify for the first time a mechanism by which rosiglitazone stimulates fatty acid oxidation in skeletal muscle, namely the chronic, subcellular relocation of FAT/CD36 to mitochondria. SN - 1469-7793 UR - https://www.unboundmedicine.com/medline/citation/18238811/Rosiglitazone_increases_fatty_acid_oxidation_and_fatty_acid_translocase__FAT/CD36__but_not_carnitine_palmitoyltransferase_I_in_rat_muscle_mitochondria_ L2 - https://doi.org/10.1113/jphysiol.2007.146563 DB - PRIME DP - Unbound Medicine ER -