scholarly journals Selective biliary lipid secretion at low bile-salt-output rates in the isolated perfused rat liver. Effects of phalloidin

1986 ◽  
Vol 237 (1) ◽  
pp. 301-304 ◽  
Author(s):  
K Rahman ◽  
R Coleman
Keyword(s):  
Bile Salt ◽  
Bile Salts ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Biliary Lipid ◽  
Perfusion Fluid ◽  
Lipid Secretion ◽  
Rat Livers ◽  
Secretion Rates ◽  
Salt Secretion

At high bile-salt-secretion rates the biliary secretion of phospholipids and cholesterol is dependent on that of the bile salts. However, at low bile-salt outputs some secretion remains. Isolated perfused rat livers were used in these experiments in order to study the bile-salt-independent secretion of biliary lipids. The livers were isolated and saline (0.9% NaCl), or phalloidin dissolved in saline, was added to the perfusion fluid after 1 h of liver isolation. The concentration and output of cholesterol was significantly decreased in phalloidin-treated livers compared with the controls, whereas there was no significant decrease in phospholipids; the secretion of cholesterol and phospholipids can thus be uncoupled from each other by the action of phalloidin. These experiments suggest that a proportion of cholesterol gets into bile independently of bile salts and phospholipids. These findings are discussed in relation to the supersaturation of some biles with cholesterol and its relationship to the bile-salt-independent fraction of cholesterol.

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.

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.

Expression of liver plasma membrane transporters in gallstone-susceptible and gallstone-resistant mice

2002 ◽  
Vol 361 (3) ◽  
pp. 673-679 ◽  
Author(s):  
Oliver MÜLLER ◽  
Carmen SCHALLA ◽  
Jürgen SCHEIBNER ◽  
Eduard F. STANGE ◽  
Michael FUCHS
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Protein Expression ◽  
Bile Salt ◽  
Membrane Transporters ◽  
Biliary Lipid ◽  
Liver Plasma Membrane ◽  
Lithogenic Diet ◽  
Secretion Rates ◽  
Salt Secretion

We tested the hypothesis that differential expression of liver plasma membrane transporters might account for variations in biliary lipid secretion rates between gallstone-susceptible C57L/J and gallstone-resistant AKR/J mice. Plasma membrane fractions and total RNA isolated from livers of mice fed with a control or lithogenic (15% fat/1.25% cholesterol/0.5% cholic acid) diet were used for measurements of steady-state gene expression of hepatobiliary transport systems for bile salts (Ntcp1/Slc10a1, Oatp1/Slc21a1 and Bsep/Abcb11), phospholipids (Mdr2/Abcb4), organic anions (Mrp2/Abcc2) and organic cations (Oct1/Slc22a1). Irrespective of the diet, the steady-state gene expression of hepatobiliary transporters did not differ significantly between the two strains. Despite a higher basal bile flow and bile-salt secretion in C57L mice, Mrp2 (Abcc2) and Bsep (Abcb11) expression did not differ between the two strains. Elevated biliary phospholipid secretion in response to the lithogenic diet was linked to increased Mdr2 (Abcb4) protein expression, whereas the induction of Oct1 (Slc22a1) might reflect an enhanced uptake of choline for augmented phospholipid synthesis. In response to the lithogenic diet, Bsep (Abcb11) protein expression was up-regulated only marginally and bile salt secretion did not increase. The down-regulation of Ntcp1 (Slc10a1) protein expression might protect hepatocytes from high intracellular bile-salt loads. We conclude that variations in protein function rather than in the gene expression of liver plasma membrane transporters might account for variations in biliary lipid secretion rates. Our findings support the concept that the formation of lithogenic bile is caused by the hypersecretion of bile salts as a result of augmented availability of canalicular membrane cholesterol, possibly amplified by bile-salt—phospholipid uncoupling due to the increased bile flow.

Effect of Lysine Acetylsalicylate on Biliary Lipid Secretion in Dogs

1975 ◽  
Vol 49 (3) ◽  
pp. 253-256 ◽  
Author(s):  
S. Erlinger ◽  
Dominique Bienfait ◽  
Renee Poupon ◽  
Micheline Dumont ◽  
M. Duval
Keyword(s):  
Bile Salt ◽  
Bile Flow ◽  
Bile Salts ◽  
Biliary Lipid ◽  
Cholesterol Gallstones ◽  
Cholesterol Saturation ◽  
Parallel Increase ◽  
Lysine Acetylsalicylate ◽  
Cholesterol Secretion ◽  
Salt Secretion

1. The influence of lysine acetylsalicylate on bile flow, erythritol clearance and bile salt, phospholipid and cholesterol secretion in bile was studied in unanaesthetized dogs fitted with a Thomas duodenal cannula. 2. Lysine acetylsalicylate induced a marked increase in bile flow and a parallel increase in erythritol clearance although the bile salt secretion remained unchanged; this suggests that the compound stimulated the formation of the canalicular (hepatocytic) bile salt-independent fraction of bile flow. 3. Lysine acetylsalicylate induced a significant decrease in biliary phospholipid and cholesterol secretion and the cholesterol saturation of bile was significantly reduced. 4. It is postulated that the decrease in phospholipid and cholesterol secretion resulted from the dilution of intracanalicular bile salts. This effect of lysine acetylsalicylate, and possibly of other bile salt-independent choleretics, may be of value in the treatment of cholesterol gallstones in man.

scholarly journals Rapid kinetic analysis of the bile-salt-dependent secretion of phospholipid, cholesterol and a plasma-membrane enzyme into bile

1984 ◽  
Vol 222 (3) ◽  
pp. 631-637 ◽  
Author(s):  
P J Lowe ◽  
S G Barnwell ◽  
R Coleman
Keyword(s):  
Plasma Membrane ◽  
Bile Salt ◽  
Kinetic Analysis ◽  
Bile Salts ◽  
Mixed Micelles ◽  
Biliary Lipid ◽  
Vesicle Traffic ◽  
Membrane Enzyme ◽  
Rat Livers ◽  
Isolated Rat

Isolated rat livers were perfused under ‘one-pass’ conditions and bile was collected at 1 min intervals. After 1 min pulse, taurocholate appeared in the collected bile within 2 min, peak output occurring 2 min later. In contrast, the increased output of phospholipids and cholesterol was slower, peak output occurring 6-11 min after the original pulse of taurocholate. These results suggest that mixed micelles cannot be formed inside the cell or during passage of bile salts through the membrane, since bile salt and lipids should then parallel each other. The bile salts must therefore be pumped into the lumen and the lipids added subsequently, due to the actions of the bile salts in the canalicular lumen. It is suggested that the biliary lipid is obtained from microdomains of biliary-type lipid in the canaliculus membrane, which are vesiculated and solubilized by the action of bile salts. It is also suggested that this biliary-type lipid is brought continuously to the membrane via vesicle traffic; this traffic is increased during increased bile-salt output, and is a process that can be inhibited by colchicine.

Bile salt dependent bile flow in the rabbit: evidence for the importance of an amiloride inhibitabie pathway

1986 ◽  
Vol 64 (10) ◽  
pp. 1316-1320 ◽  
Author(s):  
S. M. Strasberg ◽  
R. G. Ilson ◽  
C. E. Bear
Keyword(s):  
Bile Salt ◽  
Bile Flow ◽  
Bile Salts ◽  
Sodium Taurocholate ◽  
Electrolyte Transport ◽  
Cellular Processes ◽  
Electrolyte Secretion ◽  
Dependent Flow ◽  
Secretion Rates ◽  
Salt Secretion

Bile salt dependent flow and electrolyte secretion in response to two bile salts were studied in awake rabbits. It was found that sodium glycodeoxycholate had a much greater choleretic and cholioneretic efficiency than sodium taurocholate. The effect of the bile salts on flow and electrolyte secretion was not linear across the range of bile salt secretion rates studied. When amiloride was administered significant decreases in choleretic and cholioneretic efficiencies occurred, but furosemide had no effect. It is concluded that bile salts stimulate electrolyte transport via amiloride inhibitable cellular processes, and that this electrolyte transport is in part responsible for bile salt dependent bile flow.

scholarly journals Effects of organic anions on biliary lipid secretion in rats. Importance of association with biliary lipid structures

1992 ◽  
Vol 286 (1) ◽  
pp. 193-196 ◽  
Author(s):  
G Yamashita ◽  
S Tazuma ◽  
G Kajiyama
Keyword(s):  
Bile Salt ◽  
Organic Anion ◽  
Sodium Taurocholate ◽  
Organic Anions ◽  
Phenol Red ◽  
Dependent Manner ◽  
Biliary Lipid ◽  
Lipid Secretion ◽  
Biliary Lipids ◽  
Salt Secretion

This study was performed to determine the effects of various organic anions on biliary lipid secretion in rats. We infused bile-salt-pool-depleted rats with sodium taurocholate at a constant rate, with or without various organic anions: Indocyanine Green (ICG), bromosulphophthalein (BSP), BSP-glutathione and Phenol Red (PR). BSP decreased biliary secretion of cholesterol and phospholipids in a dose-dependent manner without affecting bile salt secretion (uncoupling), and this change was fully reversible. In contrast, ICG, BSP-glutathione and PR did not cause such an uncoupling of biliary lipids. In addition, the distribution pattern of each organic anion to various lipid particles was determined by gel-permeation chromatography. BSP was predominantly associated with bile salt micelles, whereas vesicular association was dominant for ICG, and both BSP-glutathione and PR formed only self-aggregations. From these data, we concluded that the uncoupling of biliary lipids from bile salt secretion by BSP resulted from the interaction between BSP and bile salt micelles in the bile canaliculus, and that this interaction inhibited the capacity of bile salts to induce the secretion of phospholipids and cholesterol.

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