Abstracts Open Access
Copyright ©The Author(s) 2000. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 2000; 6(Suppl3): 9-9
Published online Sep 15, 2000. doi: 10.3748/wjg.v6.iSuppl3.9
Bile acid formation in primary human hepatocytes
Curt Einarsson, Ewa Ellis, Anna Abrahamsson, Division of Gastroenterology and Hepatology, Department of Medicine, Karolinska Institutet at Huddinge University Hospital, SE-141 86 Stockholm, Sweden
Bo-G-ran Ericzon, Department of Transplantation Surgery, Department of Clinical Chemistry Karolinska Institutet at Huddinge University Hospital, SE-141 86 Stockholm, Sweden
Ingemar Bjrkhem, Department of Clinical Chemistry Karolinska Institutet at Huddinge University Hospital, SE-141 86 Stockholm, Sweden
Magnus Axelson, Department of Clinical Chemistry Karolinska Institutet at Karolinska University Hospital, SE-141 86 Stockholm, Sweden
Author contributions: All authors contributed equally to the work.
Correspondence to: Curt Einarsson, Division of Gastroenterology and Hepatology, Department of Medicine, Karolinska Institutet at Huddinge University Hospital, SE-141 86 Stockholm, Sweden. curt.einarsson@medhs.ki.se Fax: 8-585-823-35
Received: May 25, 2000
Revised: June 28, 2000
Accepted: July 10, 2000
Published online: September 15, 2000

Abstract

AIM: To evaluate a system for bile acid formation in human hepatocytes in comparison with HepG2 cells.

METHODS: Hepatocytes were isolated from normal human liver tissue and were cultured in serum free William’s E medium. The medium was collected and renewed every 24 h. Bile acids and their precursors in media were finally analysed by gas chromatography-mass spectrometry.

RESULTS: Cholic acid (CA) and chenodeoxycholic acid (CDCA) conjugated with glycine or taurine accounted for 70% and 25% of total steroids. One third of CDCA was also conjugated with sulphuric acid. Dexamethasone and thyroid hormone alone or in combination did not significantly affect bile acid formation. The addition of cyclosporin A (10 μm) inhibited the synthesis of CA and CDCA by about 13% and 30%, respectively.

CONCLUSION: Isolated human hepatocytes in primary culture behave as in the intact liver by converting almost quantitatively cholesterol to conjugated CA and CDCA. This is in contrast to cultured HepG2 cells, which release large amounts of bile acid precursors and unconjugated bile acids into the medium.

Key Words: Bile acid and salts, Cells, cultured, Cholesterol/metabolism, Cyclosporine, Human hepatocytes, Mass fragmentography



Footnotes

E- Editor: Hu S

$[References]