Fasting hyperbilirubinemia in Bolivian squirrel monkeys with a Gilbert's-like syndrome.
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.
Cornelius
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CE
Department of Animal Resources, Scripps Research Institute, La Jolla, California 92037.
D000818:Animals; D001663:Bilirubin / Q000378:metabolism*; D004195:Disease Models, Animal; D005215:Fasting; D005878:Gilbert Disease / Q000209:etiology*; D014453:Glucuronosyltransferase / Q000378:metabolism; D006801:Humans; D012453:Saimiri / Q000378:metabolism*
D014453:Glucuronosyltransferase; D001663:Bilirubin