Three targets of branched-chain amino acid supplementation in the treatment of liver disease
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
20071143
DOI
10.1016/j.nut.2009.06.027
PII: S0899-9007(09)00308-6
Knihovny.cz E-resources
- MeSH
- Hyperammonemia blood drug therapy MeSH
- Hepatic Encephalopathy drug therapy MeSH
- Cachexia drug therapy etiology MeSH
- Humans MeSH
- Liver Diseases blood complications drug therapy MeSH
- Dietary Supplements MeSH
- Liver Regeneration MeSH
- Amino Acids, Branched-Chain administration & dosage blood deficiency MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Amino Acids, Branched-Chain MeSH
The article explains the pathogenesis of disturbances in branched-chain amino acid (BCAA; valine, leucine, and isoleucine) and protein metabolism in various forms of hepatic injury and it is suggested that the main cause of decrease in plasma BCAA concentration in liver cirrhosis is hyperammonemia. Three possible targets of BCAA supplementation in hepatic disease are suggested: (1) hepatic encephalopathy, (2) liver regeneration, and (3) hepatic cachexia. The BCAA may ameliorate hepatic encephalopathy by promoting ammonia detoxification, correction of the plasma amino acid imbalance, and by reduced brain influx of aromatic amino acids. The influence of BCAA supplementation on hepatic encephalopathy could be more effective in chronic hepatic injury with hyperammonemia and low concentrations of BCAA in blood than in acute hepatic illness, where hyperaminoacidemia frequently develops. The favorable effect of BCAA on liver regeneration and nutritional state of the body is related to their stimulatory effect on protein synthesis, secretion of hepatocyte growth factor, glutamine production and inhibitory effect on proteolysis. Presumably the beneficial effect of BCAA on hepatic cachexia is significant in compensated liver disease with decreased plasma BCAA concentrations, whereas it is less pronounced in hepatic diseases with inflammatory complications and enhanced protein turnover. It is concluded that specific benefits associated with BCAA supplementation depend significantly on the type of liver disease and on the presence of inflammatory reaction. An important task for clinical research is to identify groups of patients for whom BCAA treatment can significantly improve the health-related quality of life and the prognosis of hepatic disease.
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