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Lithocholate metabolism in baboons fed chenodeoxycholate

R H Palmer, C K McSherry

    The Journal of Laboratory and Clinical Medicine
    |April 1, 1982
    PubMed
    Summary
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    Chenodeoxycholate causes liver damage in most species, but humans are protected by efficient lithocholate sulfation. Baboon studies show slower metabolism and larger lithocholate pools, supporting sulfation

    Area of Science:

    • Hepatology
    • Bile Acid Metabolism
    • Comparative Physiology

    Background:

    • Chenodeoxycholate administration induces hepatic lesions in many species, linked to lithocholate formation.
    • Humans exhibit resistance to these lesions, potentially due to distinct lithocholate metabolism, including enhanced sulfation and rapid elimination.

    Purpose of the Study:

    • To investigate species-specific responses to chenodeoxycholate by examining 14C-lithocholate metabolism in baboons with intact gallbladders.
    • To compare lithocholate metabolism in baboons receiving chenodeoxycholate versus controls.

    Main Methods:

    • Studied the distribution of 14C-lithocholate metabolites in bile.
    • Analyzed the kinetics of 14C-lithocholate in taurine- and glycine-conjugated pools.
    • Compared metabolic profiles and kinetic parameters between treated and control baboons.

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    Main Results:

    • Lithocholate sulfation was limited (10%) in baboons, with no significant difference between treated and control groups.
    • Treated baboons exhibited 2-3 times greater 14C-lithocholate input and pool sizes compared to controls.
    • Fractional turnover rates were slower, and pool sizes larger in baboons than in humans or cholecystectomized monkeys.

    Conclusions:

    • The findings support the hypothesis that sulfation is a key protective mechanism against lithocholate toxicity in humans.
    • Species differences in chenodeoxycholate conversion to lithocholate and subsequent absorption may also contribute to varying toxic responses.