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Am J Physiol Cell Physiol 269: C1287-C1294, 1995;
0363-6143/95 $5.00
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AJP - Cell Physiology, Vol 269, Issue 5 C1287-C1294, Copyright © 1995 by American Physiological Society

ARTICLES

Leucine activates system A amino acid transport in L6 rat skeletal muscle cells

H. E. McDowell, G. R. Christie, G. Stenhouse and H. S. Hundal
Department of Anatomy and Physiology, University of Dundee, Scotland, United Kingdom.

In this study, we present evidence showing that leucine is involved in the upregulation of system A amino acid transport activity in the L6 rat skeletal muscle cell line. At leucine concentrations of > or = 0.05 mM, the uptake of N-methylamino-alpha-isobutyric acid (MeAIB), a paradigm system A substrate, was stimulated by up to 50%. Kinetic analysis revealed that this stimulation was a result of an increase in the maximal transport rate of MeAIB uptake, from 327 +/- 26 to 450 +/- 8 pmol.min-1.mg protein-1 after incubation of cells with leucine. No significant change in the concentration at which MeAIB transport was half maximal was observed. System A activation was biphasic, reaching an initial plateau after 3 h, with a second phase of activation being observed after 5 h. The initial activation of system A transport occurred by a mechanism distinct from that activated by insulin-like growth factor-I (IGF-I) (3 nM), since the effects of leucine and IGF-I were additive. This activation was not due to transstimulation, since 2-amino-2-norbornane-carboxylic acid, a specific system L substrate, did not stimulate system A. Leucine's keto acid, ketoisocaproic acid, prevented the activation of system A transport, whereas aminooxyacetate, a transaminase inhibitor, augmented the increase in system A activity by leucine. Both cycloheximide and actinomycin D inhibited the leucine-induced increase in MeAIB uptake. The present results indicate that leucine, or some cellular component regulated by it, is capable of stimulating system A transport through control of DNA transcription, possibly of a gene encoding either a repressor or enhancer molecule of system A or perhaps of the gene encoding system A itself.


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