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Human CYP7A1 deficiency: progress and enigmas
Anne Beigneux, … , Alan F. Hofmann, Stephen G. Young
Anne Beigneux, … , Alan F. Hofmann, Stephen G. Young
Published July 1, 2002
Citation Information: J Clin Invest. 2002;110(1):29-31. https://doi.org/10.1172/JCI16076.
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Commentary

Human CYP7A1 deficiency: progress and enigmas

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Abstract

Commentary

Authors

Anne Beigneux, Alan F. Hofmann, Stephen G. Young

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Figure 1

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(a) The classical pathway for bile acid synthesis begins with CYP7A1, wh...
(a) The classical pathway for bile acid synthesis begins with CYP7A1, which converts cholesterol into 7α-hydroxycholesterol. This pathway mainly produces cholic acid in humans. (b) Alternate pathways for bile acid synthesis. Cholesterol is first converted into oxysterols by one of three different enzymes: sterol 27-hydroxylase (CYP27), expressed in multiple tissues including liver; cholesterol 25-hydroxylase, present at low levels in multiple tissues including heart, lung, and kidney; and cholesterol 24-hydroxylase (CYP46), expressed predominantly in the brain. Oxysterols are transported through the bloodstream to the liver, where they are 7α-hydroxylated by oxysterol 7α-hydroxylase (CYP7B1) in the case of 25- and 27-hydroxycholesterol and by CYP39A1 in the case of 24-hydroxycholesterol. Alternate pathways preferentially produce chenodeoxycholic acid in humans.

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