Studies on animal metabolism often require invasive interventions and may be limited in the coming years because of ethical concerns. This is the case to study in vivo metabolic processes linked to digestion, which is done with catheterized animals. Several in silico models of digestion or post-absorptive nutrient utilization have been developed, however little attention has been given to the intestinal tract itself. Therefore, our aim was to aggregate current knowledge to better understand the dynamics of metabolic fluxes of amino acids (AA) in the small intestine of pigs. A mechanistic model was built as a series of differential equations representing the metabolism of an unspecific AA in the intestine of pigs. The model was built with a series of functional intestinal segments, with an identical structure. Each segment included four state variables representing dietary proteins, luminal free AA, free AA in intestinal cells, and protein-bound AA. These state variables were linked by fluxes representing the main metabolic pathways of AA metabolism, namely hydrolysis of dietary protein, absorption of resulting AA, synthesis and degradation of cellular protein, endogenous secretions, and exchanges with blood. To parametrize the model, data were obtained from the literature and, if not available, values assumed as reasonable were used. A simulation was done with 1000 intestinal segments during a period of 24 h in which the animal received five meals followed by an overnight fast. During periods of feed intake, the model simulated the export of AA to the blood, while during fasting it simulated the importation of AA from the blood to maintain cellular homeostasis. About 30% of the absorbed AA did not appear in the blood due to their usage for synthesis of intestinal proteins. Part of these proteins were redirected to the intestinal lumen as endogenous secretions driven by the presence on intestinal content. In this version of the model, recycling of endogenous proteins was not yet considered, which led to an increase in intestinal sequestration of AA. This first model constitutes a basis for the further development as well as a tool to test hypotheses about metabolic fluxes of AA in the intestine.