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T₃ increases lactate transport and the expression of MCT4, but not MCT1, in rat skeletal muscle

¹Department of Kinesiology, University of Waterloo, Waterloo, Ontario N2L 3G1; ²Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada; and ³Department of Life Sciences (Sports Sciences), University of Tokyo, Tokyo 153, Japan

Submitted 17 February 2003 ; accepted in final form 18 April 2003

Triiodothyronine (T₃) regulates the expression of genes involved in muscle metabolism. Therefore, we examined the effects of a 7-day T₃ treatment on the monocarboxylate transporters (MCT)1 and MCT4 in heart and in red (RG) and white gastrocnemius muscle (WG). We also examined rates of lactate transport into giant sarcolemmal vesicles and the plasmalemmal MCT1 and MCT4 in these vesicles. Ingestion of T₃ markedly increased circulating serum T₃ (P < 0.05) and reduced weight gain (P < 0.05). T₃ upregulated MCT1 mRNA (RG +77, WG +49, heart +114%, P < 0.05) and MCT4 mRNA (RG +300, WG +40%). However, only MCT4 protein expression was increased (RG +43, WG +49%), not MCT1 protein expression. No changes in MCT1 protein were observed in any tissue. T₃ treatment doubled the rate of lactate transport when vesicles were exposed to 1 mM lactate (P < 0.05). However, plasmalemmal MCT4 was only modestly increased (+13%, P < 0.05). We conclude that T₃ 1) regulates MCT4, but not MCT1, protein expression and 2) increases lactate transport rates. This latter effect is difficult to explain by the modest changes in plasmalemmal MCT4. We speculate that either the activity of sarcolemmal MCTs has been altered or else other MCTs in muscle may have been upregulated.

giant vesicles; heart; monocarboxylate transporter 1 mRNA; monocarboxylate transporter 4 mRNA; monocarboxylate transporter 1 protein; monocarboxylate transporter 4 protein

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