Loading…

Amino acid repletion does not decrease muscle protein catabolism during hemodialysis

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

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology: endocrinology and metabolism 2007-06, Vol.292 (6), p.E1534-E1542
Main Authors: Raj, Dominic S. C, Adeniyi, Oladipo, Dominic, Elizabeth A, Boivin, Michel A, McClelland, Sandra, Tzamaloukas, Antonios H, Morgan, Nancy, Gonzales, Lawrence, Wolfe, Robert, Ferrando, Arny
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:1 Division of Nephrology, University of New Mexico Health Sciences Center, Albuquerque; 2 Albuquerque Academy, Albuquerque; 3 Division of Pulmonary and Critical Care, 4 General Clinical Research Center, University of New Mexico Health Sciences Center, Albuquerque, New Mexico; and 5 Department 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 Address for reprint requests and other correspondence: D. S. C. Raj, Division of Nephrology, 5th Floor ACC, 2211 Lomas Blvd. NE, Albuquerque, NM 87131-5271 (e-mail: draj{at}salud.unm.edu )
ISSN:0193-1849
1522-1555
DOI:10.1152/ajpendo.00599.2006