Carnitine movement across muscle cell membranes. Studies in isolated rat muscle |
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Authors: | Charles J. Rebouche |
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Affiliation: | Neuromuscular Disease Research Center and Department of Neurology, Mayo Foundation, Rochester, Minn. 55901 U.S.A. |
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Abstract: | l-Carnitine uptake and exodus was studied in rat extensor digitorum longus muscle in vitro. A saturable transport process was observed, which had an apparent of 60 μM and of 22 nmol/h per g tissue. Transport was inhibited by 2,4-dinitrophenol, sodium azide, anaerobiosis, ouabain, and sodium ion depletion. Analogs of l-carnitine containing a quarternary ammonium group were found to inhibit uptake (d-carnitine, γ-butyrobetaine, , choline chloride, ), while those not containing this functional group (γ-aminobutyrate, d,l-β-hydroxybutyrate) had no significant effect at concentrations 100 times the apparent of l-carnitine. Carnitine exodus from rat extensor digitorum longus muscle consisted of two phases. The rapid initial phase was attributed to leakage of l-carnitine from damaged muscle fibers, as it proceeded at nearly the same rate at 0° and 37°C, and leveled off to a rate of near zero after 1 h of incubation in vitro. The quantitatively more important phase of exodus showed a latency of 1–2 h and then proceeded at a linear rate of 40–45 nmol/h per g tissue. The results of this study support the contention that l-carnitine is taken up by a carrier-mediated, active transport system in rat extensor digitorum longus muscle. Functionally, the transport system for uptake is distinct from the process by which carnitine is lost from this muscle. |
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