Digestion affects nitrogen metabolism in fish, as both exogenous and endogenous proteins and amino acids are catabolized, liberating ammonia in the process. Here we present a model of local detoxification of ammonia by the intestinal tissue of the plainfin midshipman (Porichthys notatus) during digestion, resulting in an increase in urea excretion of gastrointestinal origin. Corroborating evidence indicated whole animal ammonia and urea excretion increased following feeding and ammonia levels within the lumen of the midshipman intestine increased to high levels (1.8 ± 0.4 μmol N g-1). We propose that this ammonia entered the enterocytes and was detoxified to urea via the ornithine urea cycle (OU-C) enzymes, as evidenced by a 1.5 – 2.9 fold post-prandial increase in glutamine synthetase activity (0.14 ± 0.05 μmol min-1g-1 and 0.28 ± 0.02 μmol min-1 g-1 vs. 0.41 ± 0.03 μmol min-1g-1) and an 8.7 fold increase in carbamoyl phosphate synthetase III activity (0.3 ± 1.2 nmol min-1g-1 vs. 2.6 ± 0.4 nmol min-1g-1). Furthermore, digestion increased urea production by isolated gastrointestinal tissue 1.7 fold supporting our hypothesis that intestinal tissue synthesizes urea in response to feeding. We further propose that the intestinal urea may have been excreted into the intestinal lumen via an apical urea transporter (UT) as visualized using immunohistochemistry. A portion of the urea was then excreted to the environment along with the feces, resulting in the observed increase in urea excretion, while another portion may have been used by intestinal ureolytic bacteria. Overall, we propose that P. notatus produces urea within the enterocytes via a functional OU-C which is then excreted into the intestinal lumen. Our model of intestinal nitrogen metabolism does not appear to be universal as we were unable to activate the OU-C in the intestine of fed rainbow trout. However, literature values suggest that multiple fish species could follow this model.