Protein metabolism in liver cirrhosis: from albumin to muscle myofibrils.

PURPOSE OF REVIEW

Liver cirrhosis in the advanced state is characterized by protein wasting, as indicated by the loss of muscle mass, hypoalbuminemia, and an abnormal amino acid profile. The protein wasting condition cirrhosis is associated with a poor prognosis and reduced survival. Poor nutrition, metabolic and hormonal abnormalities, and other disease-associated alterations may all concur to protein wasting. An understanding of the causes and mechanisms leading to protein wasting in cirrhosis may help in the development of nutritional interventions and new therapies.

RECENT FINDINGS

Albumin and muscle protein turnover in cirrhotic patients have been studied in vivo with the aid of isotope dilution techniques or organ catheterization. Albumin synthesis appears to parallel liver function, i.e. the more compromised is the liver, the less is the albumin production rate. Meal-induced albumin synthesis is impaired even in compensated cirrhotic patients. Skeletal muscle protein synthesis is diminished in cirrhosis, and total muscle protein breakdown also appears to be increased, thus explaining the reduced muscle mass. Either hormone or substrate resistance, or newly involved substances (cytokines, insulin-like growth factor 1, leptin) may play a role in the reduced synthesis of both albumin and muscle proteins in liver cirrhosis.

SUMMARY

Abnormalities of both albumin and muscle protein turnover have been demonstrated in liver cirrhotic patients. The possible role of the multiple hormonal and metabolic abnormalities of this disease, as well that of cytokines and other recently discovered substances, need to be investigated further.