Select free amino acids have been suggested to promote early satiation. Initial studies indicate that L-tryptophan may play an important role in reducing appetite. The current set of experiments examined whether dietary and intragastrically administered L-tryptophan decreases food consumption and whether this effect is specific to eating stimulated by energy (calorie) needs or by pleasant taste (reward). A link between a satiating action of L-tryptophan and activity of the anorexigenic oxytocin circuit has also been investigated. Supplementation of milk formula-based diets with tryptophan reduced energy deprivation-induced consumption of these formulas in mice. Tryptophan enrichment had no effect on water intake, which precludes the involvement of taste- or thirst-related mechanisms in tryptophan-driven hypophagia. Intragastrically administered L-tryptophan decreased deprivation-induced chow intake. It also reduced hedonics-driven consumption of palatable saccharin and milk, but not of sucrose solutions in non-deprived mice, suggesting a link with feeding reward mechanisms unrelated to sucrose. Finally, oxytocin receptor blockade with very low doses of an antagonist just prior to intragastric L-tryptophan administration, completely abolished early termination of deprivation-induced food intake by this amino acid. Overall, the data indicate that dietary supplementation and intragastric delivery of free L-tryptophan reduce eating behaviour stimulated by energy needs and palatability, and that the effect of L-tryptophan is mediated by the anorexigenic oxytocin system.