Close similarities exist in the chemical structure of fetal and adult bile pigments and mechanisms for hepatic bilirubin conjugation and transport in human and nonhuman primates. Newborn monkeys, unlike other animals, develop physiologic hyperbilirubinemia and are ideal animal models in which to investigate this developmental human disorder. Aberrations in bile pigment metabolism and compartmentalization which occur in hemolytic, hepatocellular, and obstructive diseases, closely resemble those reported in counterpart syndromes in man. Similarities also exist in the mechanisms responsible for the secretion of canalicular and ductular/ductal bile and the composition of bile. Nonhuman primates offer distinct advantages for comparative studies concerning bile pigment metabolism and the secretion of bile.