scholarly journals Placebo‐Controlled Randomized Trial of an Intestinal Bile Salt Transport Inhibitor for Pruritus in Alagille Syndrome

2018 ◽  
Vol 2 (10) ◽  
pp. 1184-1198 ◽  
Author(s):  
Benjamin L. Shneider ◽  
Cathie Spino ◽  
Binita M. Kamath ◽  
John C. Magee ◽  
Lee M. Bass ◽  
...  
Keyword(s):  
Bile Salt ◽  
Randomized Trial ◽  
Alagille Syndrome ◽  
Salt Transport ◽  
Transport Inhibitor ◽  
Bile Salt Transport

Bile salt transport in intestinal lymph of the rat

1982 ◽  
Vol 12 (1) ◽  
pp. 23-27 ◽  
Author(s):  
GEOFFREY J. BECKETT ◽  
IAIN W. PERCY-ROBB
Keyword(s):  
Bile Salt ◽  
Salt Transport ◽  
Intestinal Lymph ◽  
Bile Salt Transport

Electrogenicity of Na-coupled bile salt transport in isolated rat hepatocytes

1993 ◽  
Vol 265 (1) ◽  
pp. G73-G80
Author(s):  
S. A. Weinman ◽  
R. P. Weeks
Keyword(s):  
Bile Salt ◽  
Bile Salts ◽  
Input Resistance ◽  
Rat Hepatocytes ◽  
Salt Transport ◽  
Isolated Rat Hepatocytes ◽  
Voltage Change ◽  
Uptake Rates ◽  
Dependent Transport ◽  
Bile Salt Transport

The importance of membrane voltage in uptake of bile salts into hepatocytes is not known. Electrogenicity of the primary bile salt transport process, Na-bile salt cotransport, has been difficult to determine because the large K and Cl conductances of the sinusoidal membrane (GK and GCl, respectively) obscure any transport associated currents. In the present study hepatocytes were treated to reduce these membrane conductances and electrogenic entry of taurocholate and glycocholate was demonstrated. Intracellular voltage and resistance changes resulting from bile salt transport were measured in hepatocytes in which GK and GCl were blocked by impalement with Na acetate microelectrodes and external exposure to quinine (400 microM). This increased the cell input resistance from 153 +/- 17 to 230 +/- 17 M omega (n = 14, P < 0.001). Under these conditions, exposure to 100 microM of taurocholate or glycocholate produced Na-dependent depolarizations of 3.0 +/- 0.5 and 4.2 +/- 0.8 mV, respectively. These correspond to transport currents of 13.9 and 7.6 pA/cell, which are comparable to those predicted from known [3H]taurocholate uptake rates if one positive charge enters the cell with each bile salt molecule. Although uptake of these two bile salts was electrogenic, this was not the case for all bile salts. Na-dependent transport of taurodehydrocholate, which occurs at similar rates to that for taurocholate, produced no voltage change. The unconjugated bile salts cholate and ursodeoxycholate also produced no measurable voltage or resistance changes. In conclusion, Na-dependent uptake of taurocholate and glycocholate is electrogenic, whereas uptake of taurodehydrocholate, ursodeoxycholate, and cholate is predominantly electroneutral.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Salt Transporters: Molecular Characterization, Function, and Regulation

2003 ◽  
Vol 83 (2) ◽  
pp. 633-671 ◽  
Author(s):  
Michael Trauner ◽  
James L. Boyer
Keyword(s):  
Bile Salt ◽  
Molecular Characterization ◽  
Bile Salts ◽  
Organic Anion ◽  
Transport Proteins ◽  
Salt Transport ◽  
Transport Systems ◽  
Cholestatic Liver Disease ◽  
Bile Salt Transporters ◽  
Bile Salt Transport

Molecular medicine has led to rapid advances in the characterization of hepatobiliary transport systems that determine the uptake and excretion of bile salts and other biliary constituents in the liver and extrahepatic tissues. The bile salt pool undergoes an enterohepatic circulation that is regulated by distinct bile salt transport proteins, including the canalicular bile salt export pump BSEP (ABCB11), the ileal Na+-dependent bile salt transporter ISBT (SLC10A2), and the hepatic sinusoidal Na+- taurocholate cotransporting polypeptide NTCP (SLC10A1). Other bile salt transporters include the organic anion transporting polypeptides OATPs (SLC21A) and the multidrug resistance-associated proteins 2 and 3 MRP2,3 (ABCC2,3). Bile salt transporters are also present in cholangiocytes, the renal proximal tubule, and the placenta. Expression of these transport proteins is regulated by both transcriptional and posttranscriptional events, with the former involving nuclear hormone receptors where bile salts function as specific ligands. During bile secretory failure (cholestasis), bile salt transport proteins undergo adaptive responses that serve to protect the liver from bile salt retention and which facilitate extrahepatic routes of bile salt excretion. This review is a comprehensive summary of current knowledge of the molecular characterization, function, and regulation of bile salt transporters in normal physiology and in cholestatic liver disease and liver regeneration.

Macitentan Does Not Interfere with Hepatic Bile Salt Transport

2014 ◽  
Vol 350 (1) ◽  
pp. 130-143 ◽  
Author(s):  
Alexander Treiber ◽  
Päivi Äänismaa ◽  
Ruben de Kanter ◽  
Stephane Delahaye ◽  
Marianne Treher ◽  
...  
Keyword(s):  
Bile Salt ◽  
Salt Transport ◽  
Hepatic Bile ◽  
Bile Salt Transport

Mice lacking Mrp3 (Abcc3) have normal bile salt transport, but altered hepatic transport of endogenous glucuronides

2006 ◽  
Vol 44 (4) ◽  
pp. 768-775 ◽  
Author(s):  
Noam Zelcer ◽  
Koen van de Wetering ◽  
Rudi de Waart ◽  
George L. Scheffer ◽  
Hanns-Ulrich Marschall ◽  
...  
Keyword(s):  
Bile Salt ◽  
Salt Transport ◽  
Hepatic Transport ◽  
Bile Salt Transport
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