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PubMed1994

Artificial bile inhibits bile salt-induced gallbladder glycoprotein release in vitro.

The more hydrophobic bile salts cause rapid release of preformed gallbladder mucin and other glycoproteins by gallbladder explants in vitro, whereas the less hydrophobic bile salts elicit a lesser response. This study was designed to determine (a) whether this short-term effect was matched by a sustained increase in glycoprotein secretion over 24 hr and (b) whether it occurred when bile salts were presented in model biles rather than aqueous solution. Although 3 mmol/L taurodeoxycholate in aqueous solution increased release of preformed gallbladder glycoprotein to 843% of control values after 30 min incubation (p < 0.001), no significant increase was observed after 24 hr. The more prolonged exposure also reduced precursor uptake by 32% (p < 0.05) and inhibited synthesis of new glycoprotein by 24% (p < 0.05). Moreover, the stimulatory effect of taurodeoxycholate on release of gallbladder glycoprotein was much reduced when it was presented in model biles rather than in aqueous solution. Nor was there any difference between the effects of more hydrophobic vs. less hydrophobic bile salts when presented in model biles. Aqueous solutions of the more hydrophobic bile salts induce a rapid release of gallbladder glycoprotein in vitro but do not produce a sustained increase in glycoprotein secretion. Their effect is liable to be prevented in vivo by interaction between bile salts and the other lipids in gallbladder bile.

Animals↗

PubMed1992

Rejection of murine congenic bile ducts: a model for immune-mediated bile duct disease.

Immune-mediated injury of prenatal and postnatal extrahepatic bile duct epithelium has been poorly characterized. In a transplantation model of bile duct allografts, segments of the common bile duct from fetal day 18, postnatal day 7 and day 21, and adult (greater than 6-weeks) mice were grafted under the renal capsule of adult congenic mice. The progression of rejection injury in these bile duct allografts was then followed by histological evaluation at 1-week intervals. After 3 weeks there was a significant difference in the number of fetal congenic bile duct grafts that had maintained their luminal architecture compared with the more mature adult congenic grafts that had fibrosclerosed. The onset and progression of the rejection injury in the adult congenic bile duct grafts was associated with an induction of class I and class II histocompatibility antigen expression in the adult bile duct epithelium; the severity of this injury could be attenuated by treatment of the recipient mice with cyclosporin A. Thus, the fibrosclerosing lesion of extrahepatic ducts observed in this model of rejection injury is similar to the histopathology of neonatal biliary atresia or primary sclerosing cholangitis, and susceptibility to this injury is dependent on the age of the donor tissue. The immune nature of the injury and the ontogeny of expression of histocompatibility antigen in bile duct tissue indicate that the above factors may be important to the pathogenesis of these extrahepatic bile duct diseases. This experimental model may be used to test for novel factors that may modulate immune responses directed against extrahepatic bile duct epithelium.

Animals↗

PubMed1993

Bile acid-dependent vesicular transport of lysosomal enzymes into bile in the rat.

BACKGROUND: Bile acids may stimulate the movement of hepatocyte vesicles and enhance their fusion with the biliary canaliculus. The present study examined the effects of various bile acids on the exocytosis of the contents of hepatocyte lysosomes into the biliary canaliculus. METHODS: The effects of various bile acids on hepatocyte lysosome movement and on exocytosis of the contents of hepatocyte lysosomes into the biliary canaliculus were determined from the distribution of fluorescein isothiocyanate-dextran--labeled lysosomes in hepatocyte couplets and by quantitating biliary lysosomal enzyme output in rats. RESULTS: Hydrophobic as well as hydrophilic and nonmicellar bile acids were found to stimulate to a similar degree the output of lysosomal enzymes into bile, indicating that bile acid-induced change of canalicular or lysosomal membrane fluidity is not responsible for enhanced exocytosis. The taurocholate-dependent increase in lysosomal enzyme excretion was completely blocked by either microtubule or microfilament inhibition, suggesting that these subcellular structures are involved in bile acid-dependent vesicular transport. Fluorescent microscopy studies showed that taurocholate causes a microtubule-dependent translocation of lysosomes towards the canaliculus in hepatocyte couplets, which occurred at the same time as increased output of lysosomal enzymes into bile. CONCLUSIONS: The results suggest that bile acids modulate vesicle traffic towards the canaliculus by a mechanism unrelated to bile acid interaction with the vesicle membrane.

Actin Cytoskeleton↗

PubMed1980

Bile acids in the fetal rat: effect of maternal bile duct ligation.

The effect of bile duct ligation during pregnancy in rats (thereby increasing maternal plasma bile acids levels) on the bile acid content and composition in the fetus was examined. In spite of 30-fold increase in maternal plasma cholic acid, the bile acid content in the fetus of bile duct ligated rats was significantly lower (p less than 0.05) with a significant reduction in cholic acid content. Plasma cholesterol levels of fetuses from bile duct ligated rats were also significantly lower (p less than 0.05). In addition to the commonly expected bile acids, gas-liquid chromatographic analysis of the fetal bile acid pool showed peaks corresponding to several secondary bile acids. These results suggest that the transfer of primary bile acids of maternal origin into the fetus is minimal.

Animals↗

PubMed1999

Biliary bacterial infection decreased the secretion of bile acids and bilirubin into bile.

BACKGROUND: Bacterial cholangitis is frequently associated with serious complications. METHODS: The plasma disappearance rates and the biliary output of bile acids and bilirubin after percutaneous transhepatic biliary drainage (PTBD) were examined in 29 patients with extrahepatic biliary obstruction. RESULTS: Twenty-nine patients were divided into the bacteria-minus (n = 17) and bacteria-plus (n = 12) groups. Decreases in the plasma bile acid and bilirubin levels of the bacteria-minus group (t1/2 = 0.38 and 3.8 days for bile acids and bilirubin, respectively) were faster than those of the bacteria-plus group (t1/2 = 1.7 and 7.5 days). The bile flow rate was significantly increased in the bacteria-plus group compared with the bacteria-minus group. The calculated values of bilirubin and bile acid in the bile were higher in the bacteria-minus group than in the bacteria-plus group. CONCLUSIONS: Bacterial colonization in the bile stimulates bile duct cells to increase bile volume and inhibits the hepatocyte transport activity of bile acids and bilirubin.

Aged↗

PubMed1994

The effect of bile acid hydrophobicity on nucleation of several types of cholesterol crystals from model bile vesicles.

Nucleation of cholesterol crystals is thought to occur from cholesterol-phospholipid vesicles. We tested the hypothesis that bile acids are necessary for nucleation of cholesterol crystals. Model bile vesicles were prepared by KBr density ultracentrifugation of supersaturated model bile and mixed with one of the following bile acids: ursodeoxycholate, taurocholate, cholate, chenodeoxycholate or deoxycholate in final concentrations of 3, 30 and 100 mM. Vesicles were also mixed with various combinations of ursodeoxycholate and deoxycholate. Nucleation was assessed semi-quantitatively with polarizing microscopy. After 5 days, samples were again subjected to ultracentrifugation. Addition of 3 and 30 mM taurocholate, cholate, chenodeoxycholate and deoxycholate to vesicles induced nucleation. The extent of nucleation increased significantly with increasing bile acid hydrophobicity: deoxycholate > chenodeoxycholate > cholate > taurocholate (p < 0.05). At 100 mM bile acid this order was reversed (p < 0.05) because most of the cholesterol was solubilized in micelles as shown by ultracentrifugation after 5 days. Percentages of vesicular cholesterol decreased with increasing hydrophobicity: deoxycholate < chenodeoxycholate < cholate < taurocholate (p < 0.05). Ursodeoxycholate did not induce nucleation. At least seven cholesterol crystal shapes could be distinguished and all crystal types could be found after addition of various combinations of ursodeoxycholate+deoxycholate. We conclude that in this model: (a) bile acid species play an important role in the precipitation of cholesterol crystals from model bile vesicles; (b) the more hydrophobic bile acids induce more cholesterol crystal precipitation; and (c) the hydrophobicity of bile acids influences cholesterol crystal morphology.

Bile↗

PubMed1999

Effect of octreotide (Sandostatin 201-995) on bile flow and bile components.

Octreotide (Sandostatin 201-995) has an inhibitory effect on gastric, intestinal, and pancreatic secretions and hepatic and splachnic blood flow. We examined the effects of octreotide on bile flow and bile components in 10 patients with T-tube choledochostomy. A Fogarty balloon catheter was inserted distal to the T-tube of these patients for measurement of bile flow and bile components. Bile samples were obtained to analyze bile acid, phospholipid, lipoprotein, and cholesterol, and bile flow measurements were performed every 15 min for a period of 90 min before study and after normal saline and octreotide administrations. While octreotide had an inhibitory effect on bile flow, the concentrations of bile acid, phospholipid, and lipoprotein in bile were increased with octreotide.

Adult↗

PubMedDate not supplied

Biliary tract infection with anaerobes and the presence of free bile acids in bile.

Gallbladder bile from 24 patients (five with anaerobic biliary tract infection, 10 with aerobic biliary tract infection, and nine without biliary tract infection) was examined by thin-layer chromatography (TLC) for the presence of free bile acids. All five patients with an anaerobic biliary tract infection had small amounts of free bile acids in gallbladder bile. Seven of 10 patients with aerobic biliary tract infection and nine patients with sterile bile had no detectable free bile acids. Minute amounts of free bile acids were detectable on TLC in bile of three patients with aerobic infections. Calcium bilirubinate stones were more common in patients with free bile acids in bile.

Bacteria, Anaerobic↗

PubMed1986

Sulfated and nonsulfated bile acids in urine of patients with biliary atresia: analysis of bile acids by high-performance liquid chromatography.

To elucidate urinary bile acid patterns in patients with biliary atresia (BA), 15 sulfated and nonsulfated bile acids in urine were separately measured by high-performance liquid chromatography. This relatively simple technique for fluorescence detection utilizes the enzyme 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) to reveal urinary bile acid patterns. By this method, recovery rates of sulfated and nonsulfated bile acids in urine were satisfactory, and this analysis was shown to be applicable to clinical situations. In 10 patients with BA, the mean level of total bile acids in urine (23.35 +/- 18.51 mumol/day) was seven times higher than the mean level in eight normal infants (3.05 +/- 2.05 mumol/day). In the infants with BA, the mean level of total sulfated bile acids was about half of the total bile acid level. The main components of urinary nonsulfated bile acids in BA were glycocholic acid (6.21 +/- 5.55 mumol/day) and taurocholic acid (2.28 +/- 1.33 mumol/day), whereas the main components of the urinary sulfated bile acids were glycochenodeoxycholic acid (4.58 +/- 6.97 mumol/day) and taurochenodeoxycholic acid (3.67 +/- 3.54 mumol/day). Chenodeoxycholic acid, which is relatively toxic to the liver, may more easily be conjugated with sulfate and, hence, excreted into urine at a faster rate than cholic acid. Marked individual variations in urinary bile acid patterns were observed not only in BA patients but also in normal controls.

Adult↗

PubMed1975

Bile composition and bile cast formation after transplantation of the liver in man.

Transplantation of the liver in man is frequently complicated by biliary fistula and obstruction of the biliary tree by casts, which suggests that the composition of the bile may be abnormal. In part of the present study, bile composition was investigated in three recipients during the first few weeks after transplantation, when a T tube was in place. Supersaturation of bile with cholesterol was found in two patients immediately after surgery and during episodes of acute rejection, but bile was never lithogenic in the third. There was no evidence of bile stasis in the absence of acute rejection and bile viscosity was normal in all three patients throughout the study. Free bile acids and free bilirubin, which are relatively insoluble products of bacterial metabolism, were not present in the bile of any patient. However, chemical analysis of casts found at autopsy in a fourth recipient showed that the major component was free bilirubin. Escherichia coli was grown in cultures of the casts and the organisms were shown to possess glucuronidase activity, thus providing an explanation for the high bilirubin content. There was also some evidence in one case that damage to the bile duct mucosa has led to the precipitation of material upon it, and it is concluded that a number of factors, including infection, supersaturation with cholesterol, and mucosal damage, may be involved in bile case formation after transplantation of the liver.

Adult↗

PubMed2002

Bile stress response in Listeria monocytogenes LO28: adaptation, cross-protection, and identification of genetic loci involved in bile resistance.

Bile is one of many barriers that Listeria monocytogenes must overcome in the human gastrointestinal tract in order to infect and cause disease. We demonstrated that stationary-phase cultures of L. monocytogenes LO28 were able to tolerate concentrations of bovine, porcine, and human bile and bile acids well in excess of those encountered in vivo. Strain LO28 was relatively bile resistant compared with other clinical isolates of L. monocytogenes, as well as with Listeria innocua, Salmonella enterica serovar Typhimurium LT2, and Lactobacillus sakei. While exponential-phase L. monocytogenes LO28 cells were exquisitely sensitive to unconjugated bile acids, prior adaptation to sublethal levels of bile acids or heterologous stresses, such as acid, heat, salt, or sodium dodecyl sulfate (SDS), significantly enhanced bile resistance. This adaptive response was independent of protein synthesis, and in the cases of bile and SDS adaptation, occurred in seconds. In order to identify genetic loci involved in the bile tolerance phenotype of L. monocytogenes LO28, transposon (Tn917) and plasmid (pORI19) integration banks were screened for bile-sensitive mutants. The disrupted genes included a homologue of the capA locus required for capsule formation in Bacillus anthracis; a gene encoding the transcriptional regulator ZurR; a homologue of an Escherichia coli gene, lytB, involved in isoprenoid biosynthesis; a gene encoding a homologue of the Bacillus subtilis membrane protein YxiO; and a gene encoding an amino acid transporter with a putative role in pH homeostasis, gadE. Interestingly, all of the identified loci play putative roles in maintenance of the cell envelope or in stress responses.

Adaptation, Physiological↗

PubMed1984

Effects of bile and bile salt infusions on renal function in dogs.

A previous study in dogs indicated that 4 h of acute biliary obstruction was associated with an increment in the glomerular filtration rate (GFR), renal perfusion, and urinary sodium excretion. These effects could also be transmitted to a "recipient" dog following 2 h of cross circulation. In this study we examined the possible role of bile and bile products in reproducing these effects. The i.v. infusion of 15 mL of undiluted gallbladder bile produced a marked diuresis and natriuresis, while arterial pressure and GFR declined. Bile diluted as much as 1/100 in isotonic saline could produce an effect when infused intravenously. When bile diluted to 1/250 was infused into th left renal artery at 0.5 mL/min, a diuretic and natriuretic response was obtained. GFR and renal blood flow declined with more concentrated solutions, though blood pressure remained normal. Dialysis of bile, or prior incubation with cholestyramine or plasma, failed to uncover a renal vasodilator effect. Following the first two procedures, the diuretic properties of infused bile were lost. The infusion of small amounts of synthetic bile salts (taurocholate or glycocholate) into the left renal artery caused marked increments in urinary sodium excretion without any change in renal hemodynamics. The infusion of bilirubin was without effect on renal function. Taurine and glycine, the amino acids present in the conjugated bile acids, were injected i.v. Both caused marked diuresis and natriuresis, but only glycine increased GFR and renal perfusion. The plasma levels of these substances, however, were unchanged following 4 h of acute biliary obstruction. We conclude that while bile salts probably cause the diuresis of biliary obstruction, the mechanism for the increase in GFR has not yet been identified.

Animals↗

PubMed1984

Differing effects of hydroxy-7-oxotaurine-conjugated bile acids on bile flow and biliary lipid secretion in dogs.

The effects on bile flow and biliary lipid secretion of two taurine-conjugated 7-oxo bile acids, 3 alpha-hydroxy-7-oxocholanoyltaurine (I) and 3 alpha,12 alpha-dihydroxy-7-oxocholanoyltaurine (II), were measured in the unanesthetized, chronic bile fistula dog. Each synthetically prepared compound, or cholyltaurine as control, was infused intravenously at a physiological rate of 1 mumol X kg-1 X min-1 for randomized 90-min periods. Bile samples were collected and analyzed for biliary lipids (bile acids, phospholipid, and cholesterol) and bile acid composition. Both compounds were secreted efficiently in bile, recovery averaging 90%. The trisubstituted compound (II) induced a greater choleresis and less phospholipid and cholesterol secretion than the disubstituted compound (I) or cholyltaurine. Each oxo compound was partially reduced during hepatic passage: about 47% of I (to mostly chenodeoxycholyltaurine) and about 30% of II (to mostly cholyltaurine). The effect of the individual bile acids on biliary lipid secretion was then calculated by assuming that a) the infused bile acid induced biliary lipid secretion after its hepatic biotransformation and b) each bile acid or its biotransformation product exerted an independent effect on biliary lipid secretion (expressed as a linkage coefficient, e.g., phospholipid secretion/bile acid secretion). For phospholipid, the calculated linkage coefficient for I was 0.31; for II, 0.07. For cholesterol, the calculated linkage coefficient for I was 0.014; for II, 0.003. In vitro studies indicated that the critical micellar concentration (CMC) in 0.15 M Na+ was 22 mM for I and 40 mM for II (compared with 6 mM for cholyltaurine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Reoxygenation injury following anoxic perfusion preferentially impairs bile acid-independent bile flow.

We perfused isolated rat livers with Krebs-Ringer buffer, with no recirculation. Bile flow virtually stopped during 30 min of anoxia and resumed following reoxygenation to reach a plateau of 44% of the control level. When taurodehydrocholic acid (TDHC, 50 nmol/min/g liver) was administered during reoxygenation, bile flow increased three-fold (16.1 +/- 1.3 to 45.3 +/- 6.3 microliters/g liver). The increase in bile output with TDHC was 27.8 microliters/g liver, which was 89% of the control output. Bile acid output during this period was 1.4 mumol/g liver, which was 93% of the control level. Addition of allopurinol (50 nmol/min/g liver) without TDHC increased bile flow significantly (16.1 +/- 1.3 to 21.3 +/- 1.2 microliters/g liver), but the change was not significant when allopurinol and TDHC were given. The addition of allopurinol also reduced the cumulative release of lactate dehydrogenase from the liver during the reoxygenation period, but had no effect on hepatic adenosine triphosphate levels. Our data suggest that the bile acid-independent bile flow is sensitive to reoxygenation injury following anoxia whereas bile acid output and bile acid-dependent bile flow are resistant.

Adenosine Triphosphate↗

PubMed1988

Biliary physiology in rats with bile ductular cell hyperplasia. Evidence for a secretory function of proliferated bile ductules.

To establish the role of the biliary epithelium in bile formation, we studied several aspects of biliary physiology in control rats and in rats with ductular cell hyperplasia induced by a 14-d extrahepatic biliary obstruction. Under steady-state conditions, spontaneous bile flow was far greater in obstructed rats (266.6 +/- 51.9 microliters/min per kg) than in controls (85.6 +/- 10.6 microliters/min per kg), while excretion of 3-hydroxy bile acids was the same in the two groups. Infusion of 10 clinical units (CU)/kg per h secretin produced a minimal choleretic effect in controls (+3.8 +/- 1.9 microliters/min per kg) but a massive increase in bile flow in the obstructed animals (+127.8 +/- 34.9 microliters/min per kg). Secretin choleresis was associated with an increase in bicarbonate biliary concentration and with a decline in [14C]mannitol bile-to-plasma ratio, although solute biliary clearance significantly increased. Conversely, administration of taurocholate (5 mumol/min per kg) produced the same biliary effects in control rats and in rats with proliferated biliary ductules. In the obstructed animals, the biliary tree volume measured during taurocholate choleresis (67.4 +/- 15.8 microliters/g liver) was significantly greater than that determined during the increase in bile flow induced by secretin (39.5 +/- 10.4 microliters/g liver). These studies indicate that, in the rat, the proliferated bile ductules/ducts spontaneously secrete bile and are the site of secretin choleresis. Furthermore, because the proliferated cells expressed phenotypic traits of bile ductular cells, our results suggest that whereas under normal conditions the biliary ductules/ducts in the rat seem to contribute little to bile formation, secretion of water and electrolytes is a property of biliary epithelial cells.

Amylases↗

PubMed1993

The effect of biliary bile acid concentration and composition on the calcium level in human gallbladder bile.

We analyzed total and ionized calcium concentrations in gallbladder bile of 34 humans in four groups: 8 patients with no gallstone, 11 gallstone patients treated with no gallstone dissolution agents, 8 gallstone patients treated with chenodeoxycholic acid (CDCA) and 7 gallstone patients treated with ursodeoxycholic acid (UDCA). We found that total calcium level ranged from 1.40 to 8.01 mmol/liter, closely related to total bile acid concentration (r = 0.759). However, ionized calcium level was maintained in a narrow range of 0.25 to 1.23 mmol/liter and had no relation to total bile acid concentration. UDCA-rich bile showed relatively high level of ionized calcium. We performed ultrafiltration of bile with cut-off molecular weight 1,000 to investigate the interaction between biliary calcium and bile acid aggregates. The proportion of ultrafiltrated bile acid level to that in original bile in the UDCA group was statistically higher than the other groups. Relatively large percentage of smaller bile acid aggregates in UDCA-rich bile may impair its calcium solubility.

Bile↗

PubMed1975

Non chromatographic colorimetric assay for total taurine-conjugated bile acids: application of measurements of glycine: taurine ratio in bile.

A direct colorimetric assay for total conjugated taurine from bile-rich duodenal aspirates is described. The method is based on complete acetylation of the free hydroxyl groups by acetic anhydride at 100 degrees C. of both the tri- and di-hydroxy bile acids in Folch extracted bile samples. Taurine-conjugated bile acids are measured by ion pair formation with Azure A and subsequent extraction of the complex into the organic phase of a biphasic system. Absorption at 645 nm. of this complex directly quantifies total taurine-conjugated bile acid. Total bile acids are then estimated by the 3alpha-hydroxysteroid dehydrogenase assay. The difference between the concentration of the total conjugated bile acid and of the total conjugated taurine determines the concentration of glycine conjugates and the glycine:taurine ratio. Potentially interfering materials such as sulphalipids, certain phospholipids, and unconjugated bile acids are removed by Folch extraction. The 3-hydroxysteroid sulfates (cholesteryl sulfate, lithocholate sulfate, and glycocholate sulfate) are not measurable by heating in acetic anhydride and do not interfere. Taurolithocholate-3-sulfate, under identical conditions, gives a measurable but very low color yield and in normal physiologic concentrations would contribute negligible color. As previously reported, this assay under prescribed conditions is selective for long-chain amphipathic sulfates or sulfonates with no measurable color yield with glycine conjugates, unconjugated bile acids, free fatty acids, or lecithin. Values for glycine:taurine ratios by the above-described method in both normal bile extracts and extracts from patients with either elevated or depressed ratios relate closely to those determined by thin-layer chromatography.

Acetates↗

PubMed1991

Activities of APh, gamma-GT, GlDH and GPT and bile acid concentrations in serum after bile duct obstruction and cycloheximide in the rat.

The aim of this study was to investigate the effect of the protein synthesis inhibitor cycloheximide on the serum activities of gamma-Glutamyltransferase, Glutamate dehydrogenase and Glutamate pyruvate transaminase after bile duct obstruction in rats. The results showed that the increase of these enzyme activities after bile duct obstruction is further augmented by cycloheximide. Determinations of total bile acids in serum and liver showed that also the bile acid concentrations rise to a higher level after bile duct obstruction + cycloheximide than after bile duct obstruction alone. It is concluded that the effect of cycloheximide on the serum enzyme activities in extrahepatic cholestasis is produced via an influence on the metabolism of bile acids. This stresses the central role of bile acids for alterations of enzyme activities in extrahepatic cholestasis. Further, the effect of cycloheximide on bile acids after bile duct obstruction has not been reported before.

Alanine Transaminase↗