scholarly journals The importance of membrane microdomains for bile salt-dependent biliary lipid secretion

2018 ◽  
Vol 131 (5) ◽  
pp. jcs211524 ◽  
Author(s):  
Johannes Eckstein ◽  
Hermann-Georg Holzhütter ◽  
Nikolaus Berndt
Keyword(s):  
Bile Salt ◽  
Membrane Microdomains ◽  
Biliary Lipid ◽  
Lipid Secretion

scholarly journals Correction: The importance of membrane microdomains for bile salt-dependent biliary lipid secretion (doi:10.1242/jcs.211524)

2018 ◽  
Vol 131 (6) ◽  
pp. jcs217414
Author(s):  
Johannes Eckstein ◽  
Hermann-Georg Holzhütter ◽  
Nikolaus Berndt
Keyword(s):  
Bile Salt ◽  
Membrane Microdomains ◽  
Biliary Lipid ◽  
Lipid Secretion

Effect of glycodihydrofuisidate on sulfobromophthalein transport maximum in the hamster

1976 ◽  
Vol 231 (6) ◽  
pp. 1875-1878 ◽  
Author(s):  
Y Delage ◽  
M Dumont ◽  
S Erlinger
Keyword(s):  
Bile Salt ◽  
Transport System ◽  
Bile Salts ◽  
Sodium Taurocholate ◽  
Specific Effect ◽  
Biliary Secretion ◽  
Biliary Lipid ◽  
Lipid Secretion ◽  
Dye Transport ◽  
Cholesterol Secretion

The effect on sulfobromophathalein transport maximum (Tm) and biliary lipid secretion of sodium glyco-24,25-dihydrofusicate, a micelle-forming compound secreted into bile, has been studied in the hamster and compared to that of a physiological bile salt, sodium taurocholate. Biliary phospholipid and cholesterol secretion increased both during glycodihydrofusidate and taurocholate administration, an observation which suggest that both compounds increased th biliary secretion of micelle-forming compounds. In contrast, only taurocholate increased sulfobromophthalein Tm into bile, while glycodihydrofusidate administration decreased it. This observation suggests that the increase in sulfobromophthalein Tm observed during taurocholate administration is not the result of micellar sequestration. It could rather be the consequence of a specific effect of bile salts on the dye transport system.

scholarly journals Control of biliary phospholipid secretion. Effect of continuous and discontinuous infusion of taurocholate on biliary phospholipid secretion

1986 ◽  
Vol 234 (2) ◽  
pp. 421-427 ◽  
Author(s):  
K Rahman ◽  
T G Hammond ◽  
P J Lowe ◽  
S G Barnwell ◽  
B Clark ◽  
...  
Keyword(s):  
Animal Model ◽  
Bile Salt ◽  
Biliary Fistula ◽  
Perfused Liver ◽  
Biliary Lipid ◽  
Short Pulses ◽  
Lipid Secretion ◽  
Canalicular Membrane ◽  
Infusion Period ◽  
Salt Secretion

A major determinant of biliary lipid secretion is bile-salt secretion. Taurocholate (TC), a micelle-forming bile salt, was infused continuously at different rates in both isolated perfused livers and biliary-fistula rats. In both of these systems, infusion of TC brought about an elevated secretion of phosphatidylcholine for the duration of the TC infusion period. Initial phospholipid/bile-salt ratios in the bile were higher in the whole-animal model than in isolated livers, but at the higher infusion rates both secreted approx. 6 mol of phospholipid for every 100 mol of bile salt. The secretion of phospholipid, which was maintained even at high rates of bile-salt infusion, suggest a continuous and regulated phospholipid supply and secretion mechanism. In contrast, however, multiple short pulses of TC to the perfused liver, which brought about relatively equal biliary bile-salt output pulses, did not bring about equal phospholipid outputs, since the phospholipid peak size declined with each bile-salt pulse. These experiments taken together suggest either that a threshold (intracellular) bile-salt concentration may be required to ‘switch-on’ the phospholipid supply and that it may need to be maintained for continuous biliary phospholipid supply to the canalicular membrane.

scholarly journals Partial characterization of mechanism(s) by which sulphobromophthalein reduces biliary lipid secretion

1993 ◽  
Vol 291 (1) ◽  
pp. 173-177 ◽  
Author(s):  
G Yamashita ◽  
S Tazuma ◽  
K Horikawa ◽  
N Aihara ◽  
H Ochi ◽  
...  
Keyword(s):  
Bile Salt ◽  
Sodium Taurocholate ◽  
Bile Canaliculus ◽  
Biliary Secretion ◽  
Dependent Manner ◽  
Biliary Lipid ◽  
Sprague Dawley ◽  
Lipid Secretion ◽  
Biliary Lipids ◽  
Sprague Dawley Rats

This study was performed to explore the mechanisms by which sulphobromophthalein (BSP) reduces the secretion of biliary lipid using Sprague-Dawley rats (SDR) and mutant rats with congenital conjugated hyperbilirubinaemia bred from SDR (EHBR). We infused the bile-salt-pool-depleted rats with sodium taurocholate at a constant rate of 160 nmol/min per 100 g body wt. with BSP (12.5, 25 and 50 nmol/min per 100 g body wt.) or BSP-GSH (12.5, 25 and 50 nmol/min per 100 g body wt.). The biliary secretion of BSP and BSP-GSH was markedly impaired in EHBR as compared with that in SDR. BSP reduced the biliary secretion of cholesterol and phospholipids in a dose-dependent manner without affecting the secretion of bile salts and composition of fatty acids in phospholipids in SDR, but had no effect on lipid secretion in EHBR. In contrast, BSP-GSH had no such effect on biliary lipids, either in the SDR or EHBR. In addition, the amount of BSP in the liver of EHBR was in the same range as that of SDR. Therefore it is unlikely that an intracellular mechanism is involved in the phenomenon of uncoupling by BSP. We conclude that the uncoupling of biliary lipids from bile-salt secretion by BSP occurs at the level of the bile canaliculus following the secretion of unconjugated BSP.

Effects of sulfobromophthalein excretion on biliary lipid secretion in humans and dogs

1981 ◽  
Vol 240 (1) ◽  
pp. G85-G89
Author(s):  
E. A. Shafter ◽  
R. M. Preshaw
Keyword(s):  
Bile Salt ◽  
Lipid Composition ◽  
Control Period ◽  
Physical Interaction ◽  
Biliary Lipid ◽  
Lipid Secretion ◽  
Maximal Output ◽  
Biliary Lipid Composition ◽  
Molar Percent ◽  
Salt Secretion

The effect of sulfobromophthalein (BSP) on biliary lipid secretion was investigated in 12 cholecystectomized subjects, using a duodenal marker-perfusion technique. A 1-h basal period was followed by intravenous BSP infusion over 3 h, achieving the maximal excretory rate (Tm). The calculated Tm was not different from the measured maximal output. At BSP Tm, bile salt secretion was unchanged, but phospholipid, cholesterol, and bilirubin secretion were markedly reduced. Biliary lipid composition changed accordingly, higher molar percent bile salts but lower phospholipid and cholesterol. In six cholecystectomized dogs with chronic duodenal fistulas, bile was collected directly from the common duct while bile salt secretion was maintained by intravenous taurocholic acid infusion. After a 2-h control period, sufficient BSP was added to create either maximal (Tm) or submaximal conditions. BSP did not alter bile salt secretion but caused a dose-related decrease in phospholipid and cholesterol secretion. Bilirubin excretion was also reduced, whereas bile flow increased. Thus, BSP is hydrocholeretic but decreases phospholipid, cholesterol, and bilirubin secretion in both humans and dogs. The effect on biliary lipid composition is probably through a physical interaction with biliary micelles.

The mechanism of increased biliary lipid secretion in mice with genetic inactivation of bile salt export pump

2015 ◽  
Vol 308 (5) ◽  
pp. G450-G457 ◽  
Author(s):  
K. E. R. Gooijert ◽  
R. Havinga ◽  
H. Wolters ◽  
R. Wang ◽  
V. Ling ◽  
...  
Keyword(s):  
Protein Expression ◽  
Bile Salt ◽  
Biliary Secretion ◽  
Biliary Lipid ◽  
Bile Salt Export Pump ◽  
Human Bile ◽  
Lipid Secretion ◽  
Canalicular Transporters ◽  
Expression Potential ◽  
And Control

Human bile salt export pump ( BSEP) mutations underlie progressive familial intrahepatic cholestasis type 2 (PFIC2). In the PFIC2 animal model, Bsep−/−mice, biliary secretion of bile salts (BS) is decreased, but that of phospholipids (PL) and cholesterol (CH) is increased. Under physiological conditions, the biliary secretion of PL and CH is positively related (“coupled”) to that of BS. We aimed to elucidate the mechanism of increased biliary lipid secretion in Bsep−/−mice. The secretion of the BS tauro-β-muricholic acid (TβMCA) is relatively preserved in Bsep−/−mice. We infused Bsep−/−and Bsep+/+(control) mice with TβMCA in stepwise increasing dosages (150–600 nmol/min) and determined biliary bile flow, BS, PL, and CH secretion. mRNA and protein expression of relevant canalicular transporters was analyzed in livers from noninfused Bsep−/−and control mice. TβMCA infusion increased BS secretion in both Bsep−/−and control mice. The secreted PL or CH amount per BS, i.e., the “coupling,” was continuously two- to threefold higher in Bsep−/−mice ( P < 0.05). Hepatic mRNA expression of canalicular lipid transporters Mdr2, Abcg5, and Abcg8 was 45–55% higher in Bsep−/−mice (Abcg5; P < 0.05), as was canalicular Mdr2 and Abcg5 protein expression. Potential other explanations for the increased coupling of the biliary secretion of PL and CH to that of BS in Bsep−/−mice could be excluded. We conclude that the mechanism of increased biliary lipid secretion in Bsep−/−mice is based on increased expression of the responsible canalicular transporter proteins.

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