Cholangiocyte bile salt transporters in cholesterol gallstone-susceptible and resistant inbred mouse strains

Julia J. Liu, Jonathan N. Glickman, Anatoliy I. Masyuk, Nicholas F La Russo

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background and Aim: We investigated the dietary and gender influences on the expression and functionality of cholangiocyte bile salt transporters and development of biliary hyperplasia in cholesterol gallstone-susceptible C57L/J and resistant AKR/J mice. Methods: C57L and AKR mice were fed chow, a lithogenic diet, or a cholic acid-containing diet for 14 days. Expression of cholangiocyte bile salt transporter proteins ASBT (SLC10A2), ILBP (FABP6), and MRP3 (ABCC3) were studied by Western blot analysis. Taurocholate uptake studies were performed using microperfusion of isolated bile duct units. The pre- and post-perfusion taurocholate concentrations were analyzed by high performance liquid chromatography. Biliary proliferation in liver sections was scored. Results: The lithogenic diet induced ductular proliferation in C57L mice. On chow, SLC10A2 and ABCC3 were overexpressed in male and female C57L compared to AKR mice. A lithogenic diet reduced the expressions of FABP6 in both male and female C57L mice, SLC10A2 in female C57L mice, and ABCC3 in male C57L mice. These alterations in transporter expressions were not associated with changes in taurocholate uptake. The lithogenic diet induced biliary hyperplasia and reduced bile salt transporter expressions in C57L mice. Conclusions: Although bile salt uptake was not increased in the bile duct unit, we speculate that the biliary hyperplasia on the lithogenic diet may lead to an increase in intrahepatic bile salt recycling during cholesterol cholelithogenesis.

Original languageEnglish (US)
Pages (from-to)1596-1602
Number of pages7
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume23
Issue number10
DOIs
StatePublished - 2008

Fingerprint

Inbred Strains Mice
Gallstones
Bile Acids and Salts
Cholesterol
Inbred AKR Mouse
Diet
Taurocholic Acid
Hyperplasia
Bile Ducts
Perfusion
Cholic Acid
Recycling
Western Blotting
High Pressure Liquid Chromatography
Liver

Keywords

  • Bile salt transporters
  • Cholangiocytes
  • Cholehepatic shunting
  • Cholelithiasis
  • Cholesterol
  • Proliferation

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Cholangiocyte bile salt transporters in cholesterol gallstone-susceptible and resistant inbred mouse strains. / Liu, Julia J.; Glickman, Jonathan N.; Masyuk, Anatoliy I.; La Russo, Nicholas F.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 23, No. 10, 2008, p. 1596-1602.

Research output: Contribution to journalArticle

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AB - Background and Aim: We investigated the dietary and gender influences on the expression and functionality of cholangiocyte bile salt transporters and development of biliary hyperplasia in cholesterol gallstone-susceptible C57L/J and resistant AKR/J mice. Methods: C57L and AKR mice were fed chow, a lithogenic diet, or a cholic acid-containing diet for 14 days. Expression of cholangiocyte bile salt transporter proteins ASBT (SLC10A2), ILBP (FABP6), and MRP3 (ABCC3) were studied by Western blot analysis. Taurocholate uptake studies were performed using microperfusion of isolated bile duct units. The pre- and post-perfusion taurocholate concentrations were analyzed by high performance liquid chromatography. Biliary proliferation in liver sections was scored. Results: The lithogenic diet induced ductular proliferation in C57L mice. On chow, SLC10A2 and ABCC3 were overexpressed in male and female C57L compared to AKR mice. A lithogenic diet reduced the expressions of FABP6 in both male and female C57L mice, SLC10A2 in female C57L mice, and ABCC3 in male C57L mice. These alterations in transporter expressions were not associated with changes in taurocholate uptake. The lithogenic diet induced biliary hyperplasia and reduced bile salt transporter expressions in C57L mice. Conclusions: Although bile salt uptake was not increased in the bile duct unit, we speculate that the biliary hyperplasia on the lithogenic diet may lead to an increase in intrahepatic bile salt recycling during cholesterol cholelithogenesis.

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