Acute effects of decreased glutamine supply on protein and amino acid metabolism in hepatic tissue: a study using isolated perfused rat liver
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12898474
DOI
10.1016/s0026-0495(03)00107-0
PII: S0026049503001070
Knihovny.cz E-resources
- MeSH
- Algorithms MeSH
- Amino Acids metabolism MeSH
- Glutamine deficiency MeSH
- Enzyme Inhibitors blood MeSH
- Liver Circulation physiology MeSH
- Liver metabolism MeSH
- Keto Acids metabolism MeSH
- Rats MeSH
- Leucine metabolism MeSH
- o-Phthalaldehyde blood MeSH
- Oxidation-Reduction MeSH
- Perfusion MeSH
- Rats, Wistar MeSH
- Proteins metabolism MeSH
- Protein Biosynthesis MeSH
- In Vitro Techniques MeSH
- Amino Acids, Branched-Chain metabolism physiology MeSH
- Chromatography, High Pressure Liquid MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Amino Acids MeSH
- Glutamine MeSH
- Enzyme Inhibitors MeSH
- Keto Acids MeSH
- Leucine MeSH
- o-Phthalaldehyde MeSH
- Proteins MeSH
- Amino Acids, Branched-Chain MeSH
Glutamine deficiency, a common finding in severe illness, has a negative influence on immune status, protein metabolism, and disease outcome. In several studies, a close relationship between glutamine, branched-chain amino acid (BCAA), and protein metabolism was demonstrated. The aim of the present study was to investigate the effect of glutamine deficiency on amino acid and protein metabolism in hepatic tissue using a model of isolated perfused rat liver (IPRL). Parameters of protein metabolism and amino acid metabolism were measured using both recirculation and single pass technique with L-[1-(14)C]leucine and [1-(14)C]ketoisocaproate (KIC) as a tracer. Glutamine concentration in perfusion solution was 0.5 mmol/L in control and 0 mmol/L in the glutamine-deficient group. The net release of glutamine (about 11 micromol/g/h) and higher net uptake of most of the amino acids was observed in the glutamine-deficient group. There was an insignificant effect of lack of glutamine on hepatic protein synthesis, proteolysis, and the release of urea. However, significantly lower release of proteins by the liver perfused with glutamine-deficient solution was observed. The lack of glutamine in perfusion solution caused a significant decrease in leucine oxidation (6.66 +/- 1.04 v 13.67 +/- 2.38, micromol/g dry liver/h, P <.05) and an increase in KIC oxidation (163.7 +/- 16.5 v 92.0 +/- 12.9 micromL/g dry liver/h, P <.05). We conclude that decreased delivery of glutamine to hepatic tissue activates glutamine synthesis, decreases resynthesis of essential BCAA from branched-chain keto acids (BCKA), increases catabolism of BCKA, and has an insignificant effect on protein turnover in hepatic tissue.
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