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This Article Full Text Full Text (PDF) All Versions of this Article: 292/6/E1534    most recent 00599.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Raj, D. S. C. Articles by Ferrando, A. Search for Related Content PubMed PubMed Citation Articles by Raj, D. S. C. Articles by Ferrando, A.

Amino acid repletion does not decrease muscle protein catabolism during hemodialysis

¹Division of Nephrology, University of New Mexico Health Sciences Center, Albuquerque; ²Albuquerque Academy, Albuquerque; ³Division of Pulmonary and Critical Care, ⁴General Clinical Research Center, University of New Mexico Health Sciences Center, Albuquerque, New Mexico; and ⁵Department of Geriatrics, University of Arkansas, Little Rock, Arkansas

Submitted 9 November 2006 ; accepted in final form 29 January 2007

Intradialytic protein catabolism is attributed to loss of amino acids in the dialysate. We investigated the effect of amino acid infusion during hemodialysis (HD) on muscle protein turnover and amino acid transport kinetics by using stable isotopes of phenylalanine, leucine, and lysine in eight patients with end-stage renal disease (ESRD). Subjects were studied at baseline (pre-HD), 2 h of HD without amino acid infusion (HD-O), and 2 h of HD with amino acid infusion (HD+AA). Amino acid depletion during HD-O augmented the outward transport of amino acids from muscle into the vein. Increased delivery of amino acids to the leg during HD+AA facilitated the transport of amino acids from the artery into the intracellular compartment. Increase in muscle protein breakdown was more than the increase in synthesis during HD-O (46.7 vs. 22.3%, P < 0.001). Net balance (nmol·min^–1·100 ml ^–1) was more negative during HD-O compared with pre-HD (–33.7 ± 1.5 vs. –6.0 ± 2.3, P < 0.001). Despite an abundant supply of amino acids, the net balance (–16.9 ± 1.8) did not switch from net release to net uptake. HD+AA induced a proportional increase in muscle protein synthesis and catabolism. Branched chain amino acid catabolism increased significantly from baseline during HD-O and did not decrease during HD+AA. Protein synthesis efficiency, the fraction of amino acid in the intracellular pool that is utilized for muscle protein synthesis decreased from 42.1% pre-HD to 33.7 and 32.6% during HD-O and HD+AA, respectively (P < 0.01). Thus amino acid repletion during HD increased muscle protein synthesis but did not decrease muscle protein breakdown.

protein turnover; cytokines; end-stage renal disease; malnutrition; caspase-3; skeletal muscle