Fasting hyperbilirubinemia in Bolivian squirrel monkeys with a Gilbert's-like syndrome.

Abstract

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.

• Authors: C E Cornelius
• Journal: Advances in veterinary science and comparative medicine (Adv Vet Sci Comp Med) Vol. 37 Pg. 127-47 ( 1993) ISSN: 0065-3519 [Print] United States
• PMID: 8273512 (Publication Type: Journal Article, Review)

Chemical References

• Glucuronosyltransferase
• Bilirubin

Topics

• Animals
• Bilirubin (metabolism)
• Disease Models, Animal
• Fasting
• Gilbert Disease (etiology)
• Glucuronosyltransferase (metabolism)
• Humans
• Saimiri (metabolism)