Branched-chain amino acids as a protein- and energy-source in liver cirrhosis.

Abstract Protein-energy malnutrition (PEM) is a common manifestation in cirrhotic patients with reported incidences as high as 65–90%. PEM affects largely the patients’ quality of life and survival. Thus, diagnosis of and intervention for PEM is important in the clinical management of liver cirrhosis. Supplementation with branched-chain amino acids (BCAA) is indicated to improve protein malnutrition. As an intervention for energy malnutrition, frequent meal or late evening snack has been recently recommended. Plasma amino acid analysis characterizes the patients with liver cirrhosis to have decreased BCAA. Such reduction of BCAA is explained by enhanced consumption of BCAA for ammonia detoxication and for energy generation. Supplementation with BCAA raises in vitro the synthesis and secretion of albumin by cultured rat hepatocytes without affecting albumin mRNA expression. BCAA recover the impaired turnover kinetics of albumin both in rat cirrhotic model and in cirrhotic patients. Longer-term supplementation with BCAA raises plasma albumin, benefits quality of life issues, and finally improves survival in liver cirrhosis. Recent interests focused on the timing of administration of BCAA, since daytime BCAA are usually consumed by energy generation for physical exercise of skeletal muscles. Nocturnal BCAA seem to be more favorable as a source of protein synthesis by giving higher nitrogen balance. This minireview focuses on the basic and clinical aspects of BCAA as a pharmaco-nutritional source to control PEM in liver cirrhosis.