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Protein turnover and amino acid transport kinetics in end-stage renal disease.
Am J Physiol Endocrinol Metab 2004; 286(1):E136-43AJ

Abstract

Protein and amino acid metabolism is 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 intracellular amino acid transport kinetics and protein turnover by use of stable isotopes of phenylalanine, leucine, lysine, alanine, and glutamine before and during HD in six ESRD patients. Data obtained from amino acid concentrations and enrichment in the artery, vein, and muscle compartments were used to calculate intracellular amino acid transport and muscle protein synthesis and catabolism. Fractional muscle protein synthesis (FSR) was estimated by the precursor product approach. Despite a 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 was significantly higher than the inward transport during HD. FSR increased during HD (0.0521 +/- 0.0043 vs. 0.0772 +/- 0.0055%/h, 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 intradialytic increase in catabolism exceeded that of synthesis (57.8 +/- 13.8 vs. 28.0 +/- 8.5%, P < 0.05). Thus HD alters amino acid transport kinetics and increases protein turnover, with net increase in protein catabolism.

Authors+Show Affiliations

Division of Nephrology, University of New Mexico Health Sciences Center, 5th Floor, ACC, 2211 Lomas Boulevard NE, Albuquerque, NM 87131-5271, USA. draj@salud.unm.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

13129859

Citation

Raj, Dominic S C., et al. "Protein Turnover and Amino Acid Transport Kinetics in End-stage Renal Disease." American Journal of Physiology. Endocrinology and Metabolism, vol. 286, no. 1, 2004, pp. E136-43.
Raj DS, Zager P, Shah VO, et al. Protein turnover and amino acid transport kinetics in end-stage renal disease. Am J Physiol Endocrinol Metab. 2004;286(1):E136-43.
Raj, D. S., Zager, P., Shah, V. O., Dominic, E. A., Adeniyi, O., Blandon, P., ... Ferrando, A. (2004). Protein turnover and amino acid transport kinetics in end-stage renal disease. American Journal of Physiology. Endocrinology and Metabolism, 286(1), pp. E136-43.
Raj DS, et al. Protein Turnover and Amino Acid Transport Kinetics in End-stage Renal Disease. Am J Physiol Endocrinol Metab. 2004;286(1):E136-43. PubMed PMID: 13129859.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protein turnover and amino acid transport kinetics in end-stage renal disease. AU - Raj,Dominic S C, AU - Zager,Philip, AU - Shah,Vallbh O, AU - Dominic,Elizabeth A, AU - Adeniyi,Oladipo, AU - Blandon,Pedro, AU - Wolfe,Robert, AU - Ferrando,Arny, Y1 - 2003/09/16/ PY - 2003/9/18/pubmed PY - 2004/2/13/medline PY - 2003/9/18/entrez SP - E136 EP - 43 JF - American journal of physiology. Endocrinology and metabolism JO - Am. J. Physiol. Endocrinol. Metab. VL - 286 IS - 1 N2 - Protein and amino acid metabolism is 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 intracellular amino acid transport kinetics and protein turnover by use of stable isotopes of phenylalanine, leucine, lysine, alanine, and glutamine before and during HD in six ESRD patients. Data obtained from amino acid concentrations and enrichment in the artery, vein, and muscle compartments were used to calculate intracellular amino acid transport and muscle protein synthesis and catabolism. Fractional muscle protein synthesis (FSR) was estimated by the precursor product approach. Despite a 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 was significantly higher than the inward transport during HD. FSR increased during HD (0.0521 +/- 0.0043 vs. 0.0772 +/- 0.0055%/h, 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 intradialytic increase in catabolism exceeded that of synthesis (57.8 +/- 13.8 vs. 28.0 +/- 8.5%, P < 0.05). Thus HD alters amino acid transport kinetics and increases protein turnover, with net increase in protein catabolism. SN - 0193-1849 UR - https://www.unboundmedicine.com/medline/citation/13129859/Protein_turnover_and_amino_acid_transport_kinetics_in_end_stage_renal_disease_ L2 - http://www.physiology.org/doi/full/10.1152/ajpendo.00352.2003?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -