ABSTRACT
Interest in ammonia formation in the human intestine is centered on its role as a toxin in the pathogenesis of portal-systemic encephalopathy. Bacteria take up amino acids by kinetically defined active transport systems for structurally related amino acids. The plasma concentration of many amino acids is altered in Portal-Systemic Encephalopathy (PSE) and it is claimed that these abnormalities are important. Inhibition in the fermentation of amino acids by lactulose or other substrates could have both beneficial and detrimental effects. Bacterial decarboxylases degrade amino acids to form an amine and carbon dioxide. The experiments with N urea have shown that only 9% of fecal ammonia is derived from urea, indicating that over 90% of fecal ammonia is formed from other sources. The original theory was that lactulose favors the growth of acidophilic bacteria, such as Lactobacilli and discourages growth of putrefactive ammonia producing species.
