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. Author manuscript; available in PMC: 2020 Apr 21.
Published in final edited form as: Compr Physiol. 2019 Dec 18;10(1):21–56. doi: 10.1002/cphy.c190007

Figure 2.

Figure 2

Enterohepatic circulation of bile acids. Bile acids (BAs) are synthesized from cholesterol in the liver via the rate-limiting enzyme CYP7A1 and secreted into the bile duct by the bile salt export pump (BSEP). These BAs are then deposited into the small intestine, where they emulsify lipids and serve as signaling molecules. Luminal BAs are taken up into ileal enterocytes by the apical sodium-dependent bile acid transporter (ASBT) and exported into the portal blood by the organic solute transporter α/β heterodimer (OSTα/β). These BAs return to the liver, where they are taken into hepatocytes (mainly in the periportal region of the hepatic acinus) by the Na+-taurocholate cotransporting polypeptide (NTCP) and resecreted by BSEP. Within the enterocyte, BAs activate the farnesoid X receptor (FXR), which induces fibroblast growth factor 15/19 (FGF15/19) expression and secretion into the portal blood. FGF15/19 travels to the liver, where it binds to the FGF receptor 4 (FGFR4)/β-klotho (β-kl) complex. Activation of this complex reduces CYP7A1 expression, thus decreasing bile acid synthesis.

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