Regulation of Renal Tubular Bile Acid Transport in the Early Phase of an Obstructive Cholestasis in the Rat

2003 ◽  
Vol 95 (3) ◽  
pp. p49-p56 ◽  
Author(s):  
Jan Henrik Schlattjan ◽  
Christian Winter ◽  
Joachim Greven
Keyword(s):  
Bile Acid ◽  
Early Phase ◽  
Acid Transport ◽  
Bile Acid Transport ◽  
Obstructive Cholestasis ◽  
Renal Tubular

scholarly journals The solute carrier family 10 (SLC10): Beyond bile acid transport

2013 ◽  
Vol 34 (2-3) ◽  
pp. 252-269 ◽  
Author(s):  
Tatiana Claro da Silva ◽  
James E. Polli ◽  
Peter W. Swaan
Keyword(s):  
Bile Acid ◽  
Solute Carrier Family ◽  
Acid Transport ◽  
Bile Acid Transport ◽  
Solute Carrier

Abnormal hepatic sinusoidal bile acid transport: New insights into the pathogenesis of cholestasis?

2001 ◽  
Vol 120 (1) ◽  
pp. 321-322 ◽  
Author(s):  
Michael Trauner ◽  
Peter Fickert ◽  
Gernot Zollner
Keyword(s):  
Bile Acid ◽  
Acid Transport ◽  
Bile Acid Transport

Bile acid transport by basal membrane vesicles of human term placental trophoblast

1990 ◽  
Vol 99 (5) ◽  
pp. 1431-1438 ◽  
Author(s):  
Jose J.G. Marin ◽  
Maria A. Serrano ◽  
Mohamad Y. El-Mir ◽  
Nelida Eleno ◽  
C.A.Richard Boyd
Keyword(s):  
Bile Acid ◽  
Membrane Vesicles ◽  
Basal Membrane ◽  
Acid Transport ◽  
Bile Acid Transport

Liver disease with altered bile acid transport in Niemann-Pick C mice on a high-fat, 1% cholesterol diet

2005 ◽  
Vol 289 (2) ◽  
pp. G300-G307 ◽  
Author(s):  
Robert P. Erickson ◽  
Achyut Bhattacharyya ◽  
Robert J. Hunter ◽  
Randall A. Heidenreich ◽  
Nathan J. Cherrington
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Cholestatic Hepatitis ◽  
Diffuse Fibrosis ◽  
Acid Transport ◽  
High Fat ◽  
Bile Acid Transport ◽  
Niemann Pick

Cholestatic hepatitis is frequently found in Niemann-Pick C (NPC) disease. We studied the influence of diet and the low density lipoprotein receptor (LDLR, Ldlr in mice, known to be the source of most of the stored cholesterol) on liver disease in the mouse model of NPC. Npc1−/− mice of both sexes, with or without the Ldlr knockout, were fed a 18% fat, 1% cholesterol (“high-fat”) diet and were evaluated by chemical and histological methods. Bile acid transporters [multidrug resistance protein (Mrps) 1–5; Ntcp, Bsep, and OatP1, 2, and 4] were quantitated by real-time RT-PCR. Many mice died prematurely (within 6 wk) with hepatomegaly. Histopathology showed an increase in macrophage and hepatocyte lipids independent of Ldlr genotype. Non-zone-dependent diffuse fibrosis was found in the surviving mice. Serum alanine aminotransferase was elevated in Npc1−/− mice on the regular diet and frequently became markedly elevated with the high-fat diet. Serum cholesterol was increased in the controls but not the Npc1−/− mice on the high-fat diet; it was massively increased in the Ldlr−/− mice. Esterified cholesterol was greatly increased by the high-fat diet, independent of Ldlr genotype. γ-Glutamyltransferase was also elevated in Npc1−/− mice, more so on the high-fat diet. Mrps 1–5 were elevated in Npc1−/− liver and became more elevated with the high-fat diet; Ntcp, Bsep, and OatP2 were elevated in Npc1−/− liver and were suppressed by the high-fat diet. In conclusion, Npc1−/− mice on a high-fat diet provide an animal model of NPC cholestatic hepatitis and indicate a role for altered bile acid transport in its pathogenesis.

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