Colonic microbiota ammonia metabolism

Colonic microbiota/ammonia metabolism refers to the microbial-driven process where bacteria in the colon produce ammonia through the breakdown of dietary and systemic urea via bacterial urease activity or proteolysis. Unlike human cells, colonic bacteria possess urease, which converts urea into ammonia and carbamate. Ammonia can be incorporated into bacterial biomass and excreted in feces, or absorbed into the bloodstream, then detoxified by the liver via the urea cycle and glutamine synthesis. Disruption of this cycle can lead to hyperammonemia, implicated in hepatic encephalopathy and other systemic diseases. Therapeutic approaches include lowering ammonia production through manipulation of the microbiota (e.g., antibiotics, probiotics), use of ammonia-trapping drugs (lactulose), and fecal microbiota transplantation. Colonic ammonia metabolism is not a discrete drug target but rather a community process with multiple intervention points, most notably the bacterial urease enzyme. Elevated ammonia influences barrier integrity, immune activation, systemic and brain metabolism, and is monitored via blood and fecal ammonia assays. If a specific molecule is required, the relevant target would be bacterial urease, a key enzyme in ammonia production by colonic microbiota.

Other names

Colonic ammonia metabolismGut microbiota ammonia metabolismColonic urea breakdownColonic nitrogen metabolism

Lactulose decreases colonic pH, encourages ammonia-trapping and excretion. Rifaximin reduces ammonia production by targeting ammonia-forming bacteria. Probiotic transplantation replaces ammonia-producing bacteria with low-urease activity strains to mitigate ammonia production. Prebiotics stimulate bacterial proliferation, leading to increased nitrogen incorporation in bacteria and decreased colonic ammonia absorption.