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.