摘要
Sarcopenia,a condition of low muscle mass,quality,and strength,is commonly found in patients with chronic liver disease(CLD)and is associated with adverse clinical out-comes including reduction in quality of life,increased mor-tality,and complications.A major contributor to sarcopenia in CLD is the imbalance in muscle protein turnover wherein changes in various metabolic factors such as hyperammone-mia,amino acid deprivation,hormonal imbalance,gut dys-biosis,insulin resistance,chronic inflammation,etc.have important roles.In particular,hyperammonemia is a key mediator of the liver-gut axis and is known to contribute to sarcopenia by various mechanisms including increased ex-pression of myostatin,increased phosphorylation of eukary-otic initiation factor 2a,cataplerosis ofα-ketoglutarate,mi-tochondrial dysfunction,increased reactive oxygen species that decrease protein synthesis and increased autophagy-mediated proteolysis.Skeletal muscle is a major organ of insulin-induced glucose metabolism,and sarcopenia is closely linked to insulin resistance and metabolic syndrome.Patients with liver cirrhosis are in a hypermetabolic state that is associated with catabolism and depletion of amino acids,particularly branched-chain amino acids.Sarcopenia can have significant implications for nonalcoholic fatty liver disease,the most common form of CLD worldwide,because of the close link between metabolic syndrome and sarcope-nia.This review discusses the potential metabolic derange-ment as a cause or effect of sarcopenia in CLD,as well as interorgan crosstalk,which that might help identifying a novel therapeutic strategies.
