Abstract
Inhibition of 11β-hydroxysteroid dehydrogenase (11β-OHSD) by licorie-derived compounds and in cases of idiopathic impairment of this enzyme is known to result in hypermineralocorticoid syndromes, reflecting corticosteroid receptor activation by excess intracellular glucocorticoids. In this paper we address the question of whether or not endogenous inhibitors of 11β-OHSD exist that might cause pathological glucocorticoid metabolism. Using microsomal preparations we have demonstrated that bile acids are potent inhibitors of rat renal and human hepatic 11β-OHSD, with lithocholic acid exerting the strongest effect. The human renal enzyme is affected to a lesser extent. Serum of patients with cholestatic liver cirrhosis also inhibited 11β-OHSD activity, in parallel with total bile acid concentration. Cholesterol and its precursor lanosterol inhibited the enzymatic activity in microsomes from rat and human kidney cortex and human liver. We conclude that bile acids could contribute to the abnormalities of cortisol metabolism observed in cholestatic liver cirrhosis.
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