Urea nitrogen salvage mechanisms and their relevance to ruminants, non-ruminants and man

Abstract

Maintaining a correct balance of N is essential for life. In mammals, the major sources of N in the diet are amino acids and peptides derived from ingested proteins. The immediate endproduct of mammalian protein catabolism is ammonia, which is toxic to cells if allowed to accumulate. Therefore, amino acids are broken down in the liver as part of the ornithine-urea cycle, which results in the formation of urea - a highly soluble, biochemically benign molecule. Mammals cannot break down urea, which is traditionally viewed as a simple waste product passed out in the urine. However, urea from the bloodstream can pass into the gastrointestinal tract, where bacteria expressing urease cleave urea into ammonia and carbon dioxide. The bacteria utilise the ammonia as an N source, producing amino acids and peptides necessary for growth. Interestingly, these microbial products can be reabsorbed back into the host mammalian circulation and used for synthetic processes. This entire process is known as 'urea nitrogen salvaging' (UNS). In this review we present evidence supporting a role for this process in mammals - including ruminants, non-ruminants and man. We also explore the possible mechanisms involved in UNS, including the role of specialised urea transporters.