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1 Division of Nephrology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA
2 Albuquerque Academy, Albuquerque, NM, USA
3 Department of Surgery, University of Texas Medical Branch, Galveston, TX, USA
* To whom correspondence should be addressed. E-mail: draj{at}salud.unm.edu.
Protein and amino acid metabolism are abnormal in end-stage renal disease (ESRD). Protein turnover is influenced by transmembrane amino acid transport. The effect of ESRD and hemodialysis (HD) on intracellular amino acid transport kinetics is unknown. We studied the intracellular amino acid transport kinetics and protein turnover using stable isotopes of phenylalanine, leucine, lysine, alanine and glutamine before and during HD in six end-stage renal disease patients. Data obtained from amino acid concentrations and enrichment in the artery, vein and muscle compartments were used to calculate the intracellular amino acid transport and muscle protein synthesis and catabolism. Fractional muscle protein synthesis (FSR) was estimated by precursor product approach. Despite significant decrease in the plasma concentrations of amino acids in the artery and vein during HD, the intracellular concentrations remained stable. Outward transport of the amino acids were significantly higher than the inward transport during HD. FSR increased during HD (0.0521±0.0043 vs. 0.0772±0.0055%.h-1, p<0.01). Results derived from compartmental modeling indicated that both protein synthesis (118.3+/-20.6 vs. 146.5+/-20.6 nmol/min-1.100 ml leg-1, p<0.01) and catabolism (119.8+/- 18.0 vs. 174.0±14.2 nmol/min-1.100 ml leg-1, p<0.01) increased during HD. However, the intra-dialytic increase in catabolism exceeded that of synthesis (57.8±13.8 vs. 28.0±8.5%, p<0.05). Thus, hemodialysis alters the amino acid transport kinetics and increases protein turnover, with net increase in protein catabolism.
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