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This Article Full Text Full Text (PDF) All Versions of this Article: 577/1/433    most recent jphysiol.2006.115436v1 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 Enoki, T. Articles by Bonen, A. Search for Related Content PubMed PubMed Citation Articles by Enoki, T. Articles by Bonen, A. Related Collections Integrative

¹ Department of Life Sciences, College of Arts and Sciences, University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153, Japan
² Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1

We have examined the effects of administration of testosterone for 7 days on monocarboxylate transporter (MCT) 1 and MCT4 mRNAs and proteins in seven metabolically heterogeneous rat hindlimb muscles and in the heart. In addition, we also examined the effects of testosterone treatment on plasmalemmal MCT1 and MCT4, and lactate transport into giant sarcolemmal vesicles prepared from red and white hindlimb muscles and the heart. Testosterone did not alter MCT1 or MCT4 mRNA, except in the plantaris muscle. Testosterone increased MCT1 (20%–77%, P < 0.05) and MCT4 protein (29%–110%, P< 0.05) in five out of seven muscles examined. In contrast, in the heart MCT1 protein was not increased (P> 0.05), and MCT 4 mRNA and protein were not detected. There was no correlation between the testosterone-induced increments in MCT1 and MCT4 proteins. Muscle fibre composition was not associated with testosterone-induced increments in MCT1 protein. In contrast, there was a strong positive relationship between the testosterone-induced increments in MCT4 protein and the fast-twitch fibre composition of rat muscles. Lactate transport into giant sarcolemmal vesicles was increased in red (23%, P< 0.05) and white muscles (21%, P< 0.05), and in the heart (58%, P< 0.05) of testosterone-treated animals (P< 0.05). However, plasmalemmal MCT1 protein (red, +40%, P< 0.05; white, +39%, P< 0.05) and plasmalemmal MCT4 protein (red, +25%, P< 0.05; white, +48%, P< 0.05) were increased only in skeletal muscle. In the heart, plasmalemmal MCT1 protein was reduced (–20%, P< 0.05). In conclusion, these studies have shown that testosterone induces an increase in both MCT1 and MCT4 proteins and their plasmalemmal content in skeletal muscle. However, the testosterone-induced effect was tissue-specific, as MCT1 protein expression was not altered in the heart. In the heart, the testosterone-induced increase in lactate transport cannot be explained by changes in plasmalemmal MCT1 content, but in skeletal muscle the increase in the rate of lactate transport was associated with increases in plasmalemmal MCT1 and MCT4.

(Received 1 June 2006; accepted after revision 5 September 2006; first published online 7 September 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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