KYAT1, also known as kynurenine aminotransferase 1 or CCBL1, is a bi-functional enzyme. It plays a major role in Se-methylselenocysteine (MSC) metabolism, catalyzing transamination and beta-elimination activity with MSC as a substrate to produce methylselenol, a cytotoxic selenium metabolite causing apoptosis in cancer cells [2]. It is also involved in the kynurenine pathway, which is related to the metabolism of tryptophan and the production of neuroactive metabolites like kynurenic acid and quinolinic acid [5].

In a study on the effect of a heavy-metal mixture on neurological damage in rats, joint analysis of proteome and metabolome suggested that KYAT1 may participate in the neurological impairments induced by the heavy-metal mixture [1]. In patients with Prader-Willi syndrome, KYAT1 exhibited differential expression in liver steatosis, with a progressive increase from grade 1 to grade 3, indicating its potential as a biomarker for this condition [3]. In critical illness, the mRNA expression of KYAT1 in skeletal muscle was affected, and lower expression was associated with a lower risk of weakness [4].

In conclusion, KYAT1 is involved in important metabolic pathways such as the metabolism of selenium-containing compounds and the kynurenine pathway. Its role has been implicated in various disease-related processes including neurological impairments, hepatic steatosis in Prader-Willi syndrome, and critical illness-related muscle conditions, highlighting its significance in understanding these biological and disease states.