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. Author manuscript; available in PMC: 2016 May 27.
Published in final edited form as: Adv Pharmacol. 2015 May 27;74:263–302. doi: 10.1016/bs.apha.2015.04.003

Figure 1. Bile acid synthetic pathways and bile acid structure.

Figure 1

Cholesterol is the common precursor for bile acid synthesis via two major bile acid biosynthetic pathways. In the classic pathway, the rate-limiting enzyme cholesterol 7α-hydroxylase (CYP7A1) in the endoplasmic reticulum converts cholesterol into 7α-hydroxycholesterol. The 3β-hydroxysteroid dehydrogenase (3βHSD, HSD3B7) converts 7α-hydroxycholesterol to 7α-hydroxy-4 cholesten-3-one (C4). C4 can be converted to cholic acid (CA) which requires the sterol 12α-hydroxylase (CYP8B1). Without 12α-hydroxylation by CYP8B1, C4 is eventually converted to chenodeoxycholic acid (CDCA). In the classic pathway, the mitochondrial sterol 27-hydroxylase (CYP27A1) catalyzes the steroid side-chain oxidation in both CA and CDCA synthesis. In the alternative pathway, CYP27A1 catalyzes the first step to convert cholesterol to 27-hydroxycholesterol. Oxysterol 7α-hydroxylase (CYP7B1) catalyzes hydroxylation of 27-hydroxycholesterol to 3β, 7α-dihydroxy-5-cholestenoic acid, which eventually is converted to CDCA. In the large intestine, bacterial 7α-dehydroxylase removes a hydroxyl group from C-7 and converts CA to deoxycholic acid (DCA) and CDCA to lithocholic acid (LCA). In mouse liver, most of CDCA is converted to α- and β-muricholic acid (MCA).