Properties of carnitine transport in rat kidney cortex slices |
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Authors: | Peter J Huth Austin L Shug |
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Institution: | 1. Metabolic Research Laboratory, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705 U.S.A.;2. Department of Nutritional Sciences, University of Wisconsin, Madison, WI 53706 U.S.A. |
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Abstract: | The properties of carnitine transport were studied in rat kidney cortex slices. Tissue: medium concentration gradients of 7.9 for L-methyl-14C]carnitine were attained after 60-min incubation at 37°C in 40 μM substrate. L- and D-carnitine uptake showed saturability. The concentration curves appeared to consist of (1) a high-affinity component, and (2) a lower affinity site. When corrected for the latter components, the estimated Km for L-carnitine was 90 μM and per ml intracellular fluid; for D-carnitine, and per ml intracellular fluid. The system was stereospecific for L-carnitine. The uptake of L-carnitine was inhibited by (1) D-carnitine, γ-butyrobetaine, and (2) acetyl-L-carnitine. γ-Butyrobetaine and acetyl-L-carnitine were competitive inhibitors of L-carnitine uptake. Carnitine transport was not significantly reduced by choline, betaine, lysine or γ-aminobutyric acid. Carnitine uptake was inhibited by 2,4-dinitrophenol, carbonyl cyanide , N2 atmosphere, KCN, , low temperature (4°C) and ouabain. Complete replacement of Na+ in the medium by Li+ reduced L- and D-carnitine uptake by 75 and 60%, respectively. Complete replacement of K+ or Ca2+ in the medium also significantly reduces carnitine uptake. Two roles for the carnitine transport system in kidney are proposed: (1) a renal tubule reabsorption system for the steady-state maintenance of plasma carnitine; and (2) maintenance of normal carnitine levels in kidney cells, which is required for fatty acid oxidation. |
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Keywords: | Carnitine transport Renal tubule (Kidney cell) |
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