Effects of N‐acetyl‐L‐tryptophan on desorption of the protein‐bound uremic toxin indoxyl sulfate and effects on uremic sarcopenia

Abstract

AbstractIntroductionIndoxyl sulfate (IS) is a protein‐bound uremic toxin that causes uremic sarcopenia. IS has poor dialysis clearance; however, the addition of a binding competitor improves its removal efficiency.MethodsDialysis experiments were performed using N‐acetyl‐l‐tryptophan (L‐NAT) instead of l‐tryptophan (Trp) using pooled sera obtained from dialysis patients. The molecular structures of L‐NAT and Trp were similar to that of IS. Therefore, we examined whether Trp and L‐NAT were involved in muscle atrophy in the same manner as IS by performing culture experiments using a human myotube cell line.ResultsThe removal efficiency of L‐NAT was the same as that of Trp. However, L‐NAT concentrations in the pooled sera increased at the end of the experiment. Trp (1 mM) decreased the area of human myocytes, similar to IS, whereas L‐NAT did not.ConclusionL‐NAT is a binding competitor with the ability to remove protein‐bound IS while preventing sarcopenia.