4.6 Article

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

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AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00069.2003

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

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Triiodothyronine (T-3) regulates the expression of genes involved in muscle metabolism. Therefore, we examined the effects of a 7-day T-3 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 T-3 markedly increased circulating serum T-3 (P < 0.05) and reduced weight gain (P < 0.05). T-3 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. T-3 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 T-3 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.

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