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Hepatol Commun ; 5(4): 629-633, 2021 04.
Article in English | MEDLINE | ID: mdl-33860121

ABSTRACT

Organic anion transporting polypeptide (OATP) 1B1 (gene, solute carrier organic anion transporter family member 1B1 [SLCO1B1]) and OATP1B3 (SLCO1B3) serve as transporters for hepatic uptake of important endogenous substances and several commonly prescribed drugs. Inactivation of both proteins together causes Rotor syndrome. How this OATP1B1/1B3 defect disturbs bile acid (BA) metabolism is largely unknown. In this study, we performed detailed BA analysis in 3 patients with genetically diagnosed Rotor syndrome. We found that BAs glucuronidated at the C-3 position (BA-3G) accounted for 50% or more of total BAs in these patients. In contrast but similarly to healthy controls, only trace amounts of BA-3G were detected in patients with constitutional indocyanine green excretory defect (OATP1B3 deficiency) or sodium-taurocholate cotransporting polypeptide (NTCP; gene, solute carrier family 10 member 1 [SLC10A1]) deficiency. Therefore, substantial amounts of BA-3G are synthesized in hepatocytes. The cycling pathway of BA-3G, consisting of excretion from upstream hepatocytes and uptake by downstream hepatocytes by OATP1B1/1B3 may exist to reduce the burden on upstream hepatocytes. Conclusion: Detailed BA analysis revealed glucuronidated bile acidemia in patients with Rotor syndrome. Further exploration of the physiologic role of glucuronidated BAs is necessary.


Subject(s)
Bile Acids and Salts/blood , Hepatocytes/metabolism , Hyperbilirubinemia, Hereditary/metabolism , Organic Anion Transporters/metabolism , Solute Carrier Organic Anion Transporter Family Member 1B3/metabolism , Aged , Aged, 80 and over , Child , Female , Hepatocytes/pathology , Humans , Hyperbilirubinemia, Hereditary/blood , Hyperbilirubinemia, Hereditary/pathology , Infant , Male , Middle Aged , Organic Anion Transporters/blood , Solute Carrier Organic Anion Transporter Family Member 1B3/blood
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