COMMENTARY

Liver

Inappropriate ileal conservation of bile acids in cholestatic liver disease: homeostasis gone awry

A F Hofmann

Division of Gastroenterology, Department of Medicine, University of California, San Diego 92093–0813, USA; ahofmann@ucsd.edu

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Patients with cholestatic liver disease are likely to inappropriately conserve bile acids. Ursodiol corrects the defect, but is this enough?

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Keywords: electron spin resonance; experimental colitis; nitroxide radical; sulfhydryl compounds; trinitrobenzene sulphonic acid; transforming growth factor beta; neuroendocrine tumour; enteroendocrine cells; menin; Smad3; primary biliary cirrhosis; bile acids; liver disease

The first 150 words of the full text of this article appear below.

Conjugated bile acids are water soluble amphipathic end products of cholesterol metabolism that promote lipid transport in the biliary tract and small intestine by forming mixed micelles.¹ Bile acids are formed in pericentral hepatocytes by a complex multienzyme process whose details have at last been largely elucidated.² After formation, their acidic group is linked ("conjugated") with the amino group of glycine or taurine in an amide bond that is resistant to the proteolytic enzymes present in pancreatic secretion and on the surface of the enterocyte brush border. Conjugated bile acids differ from unconjugated bile acids in being membrane impermeable and water soluble at the pH conditions prevailing in the biliary tract and small intestine.

Efficient ileal conservation of bile acids results in the accumulation of a mass of bile acids termed the bile acid "pool". Between meals, most of the pool is stored in the gall bladder; with meals, . . . [Full text of this article]

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This article has been cited by other articles:

• Lefebvre, P., Cariou, B., Lien, F., Kuipers, F., Staels, B. (2009). Role of Bile Acids and Bile Acid Receptors in Metabolic Regulation. Physiol. Rev. 89: 147-191 [Abstract] [Full Text]