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The suggested pathogenic mechanisms include increased flux of HIS through HIS degradation pathway (increases in ammonia and glutamate), increased ammonia detoxification to glutamine and exchange of the BCAA with glutamine via L-transporter system in muscles (increase in glutamine and decrease in BCAA), and tetrahydrofolate depletion (decrease in glycine). Increased alanine concentration is explained by enhanced synthesis in extrahepatic tissues and impaired transamination in the liver. Increased ammonia and glutamine and decreased BCAA levels in HIS-treated subjects indicate that HIS supplementation is inappropriate in patients with liver injury. The studies investigating the possibilities to elevate carnosine (\u03b2-alanyl-L-histidine) content in muscles show positive effects of \u03b2-alanine and inconsistent effects of HIS supplementation. Several studies demonstrate HIS depletion due to enhanced availability of methionine, glutamine, or \u03b2-alanine.<\/jats:p>","DOI":"10.33549\/physiolres.934449","type":"journal-article","created":{"date-parts":[[2020,8,27]],"date-time":"2020-08-27T07:12:40Z","timestamp":1598512360000},"page":"555-564","source":"Crossref","is-referenced-by-count":28,"title":["Influence of Histidine Administration on Ammonia and Amino Acid Metabolism: A Review"],"prefix":"10.33549","author":[{"given":"M","family":"Hole\u010dek","sequence":"first","affiliation":[{"name":"Charles University, Faculty of Medicine in Hradec Kr\u00e1lov\u00e9, \u0160imkova 870, 500 03 Hradec Kr\u00e1lov\u00e9, Czech Republic. 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