Fasting unconjugated hyperbilirubinemia in Bolivian squirrel monkeys is most likely due to two mechanisms. First, a twofold increase in bilirubin production/turnover occurs during fasting. Increased bilirubin production is subsequently accompanied by increased amounts of unconjugated bilirubin in the hepatic cytosol, which requires conjugation for excretion. The presence of a twofold greater concentration of bilirubin in the livers of fed BoSM with the Gilbert's-like syndrome than in fed control Brazilian squirrel monkeys (BrSM) clearly establishes the presence of an innate subspecies difference, even without the effects of fasting. A second mechanism, which is responsible in part for FH in BoSM, is the presence of a hepatic enzyme, UDP-glucuronyl transferase, which has a higher apparent UDPGAKm and a lower Vm; this results in higher steady-state plasma and hepatic bilirubin levels during a fast when hepatic UDP-glucuronic acid levels are low. The BoSM provides the investigator with an excellent animal model for human Gilbert's syndrome type I in which to study rate-limiting mechanisms in the transport of bilirubin from plasma to bile.