Clin Mol Hepatol.  2019 Sep;25(3):270-279. 10.3350/cmh.2019.0015.

Sarcopenia: Ammonia metabolism and hepatic encephalopathy

Affiliations
  • 1Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India. ankur.jindal3@gmail.com

Abstract

Sarcopenia (loss of muscle mass and/or strength) frequently complicates liver cirrhosis and adversely affects the quality of life; cirrhosis related liver decompensation and significantly decreases wait-list and post-liver transplantation survival. The main therapeutic strategies to improve or reverse sarcopenia include dietary interventions (supplemental calorie and protein intake), increased physical activity (supervised resistance and endurance exercises), hormonal therapy (testosterone), and ammonia lowering agents (L-ornithine L-aspartate, branch chain amino acids) as well as mechanistic approaches that target underlying molecular and metabolic abnormalities. Besides other factors, hyperammonemia has recently gained attention and increase sarcopenia by various mechanisms including increased expression of myostatin, increased phosphorylation of eukaryotic initiation factor 2a, cataplerosis of α ketoglutarate, mitochondrial dysfunction, increased reactive oxygen species that decrease protein synthesis and increased autophagy-mediated proteolysis. Sarcopenia contributes to frailty and increases the risk of minimal and overt hepatic encephalopathy.

Keyword

Sarcopenia; Hepatic encephalopathy; Liver cirrhosis; Ammonia; Testosterone

MeSH Terms

Ammonia*
Aspartic Acid
Fibrosis
Hepatic Encephalopathy*
Hyperammonemia
Liver
Liver Cirrhosis
Metabolism*
Motor Activity
Myostatin
Peptide Initiation Factors
Phosphorylation
Proteolysis
Quality of Life
Reactive Oxygen Species
Sarcopenia*
Testosterone
Ammonia
Aspartic Acid
Myostatin
Peptide Initiation Factors
Reactive Oxygen Species
Testosterone
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