Effect of liver cirrhosis on phenylalanine and tyrosine metabolism

Abstract

Phenylalanine hydroxylation in vivo appears to represent a regulatory step of phenylalanine disposal and tyrosine production under acute and/or extreme conditions.

Multivariate metabotyping of plasma predicts survival in patients with decompensated cirrhosis

“…Hepatic ischaemia and failure to clear (as well as increased production of) lactate are well described and lactate is a classic biomarker of mortality in hepatology and critical illness when aerobic metabolism is overwhelmed. Increases in aromatic amino acids are also well described as ammonia levels rise in conjunction with failure of the urea cycle in patients with HE and liver failure [55] . However, ammonia alone is a poor biomarker of survival in cirrhosis as a number of cofactors including inflammation [56] are required to generate high grade HE and contribute to poor outcome.…”

The dietary protein paradox and threonine 15N‐depletion: Pyridoxal‐5'‐phosphate enzyme activity as a mechanism for the δ15N trophic level effect

“…It is suggested that the lack of significant 15 N‐fractionation for Phe is the result of its metabolic pathways that do not result in cleavage or formation of its nitrogen bonds . However, hair δ 15 N Phe values were found to be significantly higher in cirrhotic patients than in healthy individuals, and this is possibly associated with a specific increase in the release of Phe from endogenous protein breakdown during liver disease . Thus, δ 15 N Phe values can be altered by chronic disease states that affect the enzyme activities of the liver, independent of dietary intake, and this should be kept in mind for δ 15 N AA research.…”

Evidence of Active Pro-Fibrotic Response in Blood of Patients with Cirrhosis

“…Severity of liver fibrosis in known to be associated to alterations in the metabolome[ 26 ][ 27 ][ 28 ]. According to this, our work demonstrates that cirrhosis induces a wide re-programming of transcriptomic signatures involved in metabolism, as evidenced by the observed alterations in the pathways participating in aminoacid, nucleotide and arachidonic acid metabolism.…”