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At least 613 records · Page 34Linked to original sources
PubMed1979

The effects of a high-fiber diet on bile acid pool size, bile acid kinetics, and biliary lipid secretory rates in the morbidly obese.

A high-fiber diet has been suggested as one reason for the low incidence of gallstones in some populations. Therefore the authors tested the effects of a high-fiber diet on biliary secretory kinetics and bile salt kinetics in morbidly obese volunteers. Bile salt pool sizes were reduced by 50%, and their half-lives were decreased 70% after the subjects had spent 6 weeks on the high-fiber diet. Bile acid enterohepatic circulation times also were shortened dramatically. However, the lithogenicity of bile did not decrease, and bile remained supersaturated with with cholesterol. Fasting bile samples tended to be even more lithogenic than before the subjects follwed the diet. In these obese subjects, a high-fiber diet failed to reduce the tendency to secrete cholesterol-saturated bile.

Adult↗
PubMed1973

Sex differences in the bile acid composition of human bile: studies in patients with and without gallstones.

The bile acid composition of human gallbladder bile was studied in 83 subjects, 20 of each sex without discernible hepatobiliary disease, and 20 men and 23 women with cholelithiasis. The bile acids were measured by combined thin-layer and gas-liquid chromatography.In the bile of patients without cholelithiasis the molar percent of cholic acid was significantly greater in men while that of chenodeoxycholic acid was significantly greater in women.In the bile of patients with cholelithiasis the concentration of total bile acids was reduced in both sexes but there was no sex difference in the molar percent of any of the bile acids. The molar percent of CDCA (both glycine and taurine conjugates) was reduced in women, while the molar percent of CA (only the glycine conjugate) was reduced in men.

Bile↗
PubMed1979

[Effect of metyrapone on bile flow and bile acid excretion in Wistar rats].

The influence of metyrapone on bile flow and excretion of mono-(MBA), di-(DBA) and trihydroxy-(TBA)-bile acids was investigated in adult male Wistar rats after single and repeated pretreatment. MBA were not found in the rat bile. Metyrapone administration (200 mg/kg b.w. i.p.) 1 h before onset of a 3-hour bile collection period diminished bile flow and excretion of DBA and TBA. The relation TBA/DBA was changed towards DBA. Similar results were found after repeated administration 12 h after the last metyrapone injection (4 x 50 mg/kg b.w. i.p. per day for 4 consecutive days). But 60 h after the last metyrapone administration bile flow and the excretion of TBA were enhanced and the TBA/DBA ratio was changed towards TBA. The possible influence of metyrapone on bile acid hydroxylation is discussed and compared with metyrapone action on hydroxylation of foreign compounds.

Animals↗
PubMed1978

Acute hemorrhagic pancreatic necrosis in mice bile acids in gallbladder bile, serum and pancreas.

Mice develop acute hemorrhagic pancreatic necrosis with fat necrosis after 4 days of feeding on a choline deficient-ethionine supplemented (CDE) diet. The diameter, weight and histopathology of the gallbladder were determined in mice fed laboratory chow (LC), a choline-supplemented (CS) diet, a choline-deficient (CD) diet, or the CDE diet for 1, 2 or 3 days. A progressive distension of the gallbladder due to accumulation of bile, was observed in mice fed the CS, CD and CDE diets. An analysis of the bile acid composition of the pancreas, serum and gallbladder bile of mice fed the same diets for 3 days was performed. No differences between control and experimental animals were seen in the concentration and distribution of bile acids in the pancreas. It is concluded that: 1) alterations in bile acid constituents are produced by the diets; and, 2) regurgitation of bile into the pancreas of mice fed the CDE diet does not occur. Thus, bile acids do not seem to initiate or participate in the extensive cellular damage that precedes and accompanies the onset of acute hemorrhagic pancreatic necrosis with fat necrosis in mice fed the CDE diet.

Animals↗
PubMed1981

Studies on steroids. CLXX. Separation and determination of bile acid 3-sulfates in human bile by high-performance liquid chromatography.

A method for the simultaneous determination of sulfated bile acids in human bile without prior hydrolysis and solvolysis is described. The sulfate fraction was obtained from a bile specimen by passing it through a Sep-Pak C18 cartridge, followed by group separation by ion-exchange chromatography on a lipophilic gel, piperidinohydroxypropyl Sephadex LH-20. Subsequent resolution into the 3-sulfates of unconjugated, glycine- and taurine-conjugated ursodeoxycholate, cholate, chenodeoxycholate, deoxycholate and lithocholate was attained by high-performance liquid chromatography (HPLC) on an SC-02 column. Separation of these sulfates was effected when acetonitrile-0.5% ammonium carbonate (8:31, 8:26 and 8:23, v/v) was used as mobile phase. The sulfated bile acids in human bile were unequivocally identified on the basis of their behaviour in HPLC using mobile phases of various PH values. The present method proved to be applicable to the characterization and quantitation of sulfated bile acids in human bile.

Bile↗
PubMed1994

Effects of lovastatin and chenodiol on bile acid synthesis, bile lipid composition, and biliary lipid secretion in healthy human subjects.

To assess the relationship between cholesterol synthesis and feedback inhibition of bile acid synthesis, we studied seven normal human subjects taking three different doses of chenodiol, 0, 5, and 15 mg/kg per day: once while taking no lovastatin and again while taking lovastatin 80 mg/day. Lovastatin and both doses of chenodiol significantly lowered bile acid synthesis measured by the 14CO2 method, but there was no significant interaction between the perturbations. Both also lowered cholesterol saturation index of gallbladder bile without appreciable interaction, and the combination was distinctly more effective than either medication alone. Lovastatin and low-dose chenodiol both lowered biliary cholesterol secretion without affecting bile acid secretion. Increasing the dose of chenodiol did not further lower cholesterol secretion, but did further reduce saturation index because of an increase in secretion of bile acid and phospholipid. These studies indicate that there is no interaction between cholesterol synthesis and feedback return of bile acid in the enterohepatic circulation with respect to either bile acid synthesis or biliary lipid secretion; that the combination of chenodiol and lovastatin is better than either alone for improving biliary cholesterol saturation; and that the mechanism by which chenodiol lowers cholesterol saturation is dose-dependent.

Aged↗
PubMedDate not supplied

Is intracellular pH and/or intracellular bicarbonate a determinant of bile salt independent canalicular bile formation? The subject revisited.

Canalicular bile formation is a complex process that involves basolateral and apical cell membrane transport, paracellular transport and vesicular transport, all of which may be subject to regulation by pH. We review the concept that apical cell membrane bicarbonate secretion promotes bile salt independent canalicular bile formation. We show that the presence of paracellular electrolyte transport imposes a severe restriction in interpreting data from ion substitution experiments aimed at demonstrating pH or bicarbonate dependent bile formation. Furthermore, we report on experiments that all show stimulation of bile flow under three disparate experimental conditions: i) intracellular alkalinization in the absence of [HCO3-]i or associated with a decrease of [HCO3-]i, ii) intracellular alkalinization with an increase of [HCO3-]i, and iii) intracellular acidification with increase of [HCO3-]i. It is suggested that both, intracellular pH and intracellular bicarbonate may modulate canalicular bile salt independent bile formation, but it remains conjectural which mechanism is the prevailing one under a given experimental setting.

Animals↗
PubMed1987

Coexistent carcinoma in congenital dilatation of the bile duct and anomalous arrangement of the pancreatico-bile duct. Carcinogenesis of coexistent gall bladder carcinoma.

From 1972 to 1985, 40 cases of congenital dilatation of the bile duct (CDBD) were experienced in the department of the authors. Those consisted of 19 cases of anomalous arrangement of the pancreatico-bile duct (P-B anomaly), five of bile duct carcinoma, and two of gall bladder carcinoma. In addition, four patients who showed no dilatation of the bile duct in spite of the presence of a P-B anomaly were experienced, and coexistent gall bladder carcinoma was present in three of four cases. The incidence of bile duct carcinoma associated with CDBD is very high. However, coexistent gall bladder carcinoma in CDBD is a new topic, and coexistent intrahepatic bile duct carcinoma in CDBD is extremely rare. This report presents interesting and rare cases of coexistent carcinomas in these anomalies and investigates their carcinogenesis, particularly that of gall bladder carcinoma.

Adenocarcinoma, Papillary↗
PubMed2000

Altered bile composition in the gallbladder and common bile duct of patients with anomalous pancreaticobiliary ductal junction.

The high incidence of biliary tract carcinoma in patients with anomalous pancreaticobiliary ductal junction (APBDJ) has been well documented. Elevation of the secondary and free bile acid (FBA) concentrations is considered a risk factor for biliary carcinogenesis in these patients. Bile from the gallbladder and common bile duct in 12 patients with APBDJ was analyzed and compared with gallbladder bile from 19 patients with gastric cancer and a normal hepatobiliary tract. The concentrations of secondary bile acids were significantly lower in the APBDJ group than in the control group, and FBA concentrations were not detected in the gallbladder in either group. The lysolecithin (LL) in the phospholipid, which is produced from lecithin by activated phospholipase A(2) in refluxing pancreatic juice, was significantly elevated in the APBDJ group. Elevation of the LL concentration in the bile is one of the factors for the development of biliary tract carcinoma in patients with APBDJ.

Adolescent↗
PubMedDate not supplied

Analysis of bile acids and bile alcohols in urine by capillary column liquid chromatography-mass spectrometry using fast atom bombardment or electrospray ionization and collision-induced dissociation.

Solid-phase extraction and group separation by anion exchange chromatography were combined with capillary column liquid chromatography-mass spectrometry (LC/MS) to permit a thorough characterization of bile acids and intact conjugates of bile alcohols in human urine. Groups of compounds were separated according to acid strength and were analysed on a capillary column, 0.25 x 500 mm, packed with 5 microns particles of Chromasil C18, and connected via a fused silica capillary to the continuous-flow fast atom bombardment (CF-FAB) or electrospray (ES) sources of an AutoSpec-TOFFPD hybrid mass spectrometer. Acetonitrile:water mixtures containing 30 mM ammonium acetate pH 7.2 were used as mobile phases, with 5% glycerol added for FAB Ionisation. Bile acids were analysed directly or after derivatization of carboxyl groups with 4-aminobenzenesulphonic acid. Negative-ion spectra (m/z 1000 or 800 to 300 or 100) were recorded using the point detector or, in the case of ES ionization, the focal plane array detector (FPD). Deprotonated molecules of bile acids containing a sulphonic acid group were detected with a spectral signal to noise ratio of 5:1 when about 90 fmol were injected onto the column of the LC/CF-FAB system. The corresponding peak in the reconstructed ion chromatogram gave a signal-to-noise ratio of about 25:1. The sensitivity could be increased 20-50 times by using ES ionization and the FPD. Bile acids without a sulphonic acid group gave about 70% of the signal of sulphonic acids using ES ionization. The capillary column LC/MS systems were evaluated by analyses of urine from an infant with cholestatic liver disease. More than 150 different bile acids and bile alcohol conjugates were detected, some of which were partially characterized using collision induced dissociation (CID) of the deprotonated molecules and B/E linked scans. A number of compounds were detected for the first time, e.g. di-, tri-, and tetra-hydroxycholestanoic acids conjugated with N-acetylhexosamine and cholestenediol, cholestenetriol and cholestanetriol doubly conjugated with sulphuric acid and glucuronic acid. The relative merits of ES and FAB ionization are discussed.

Alcohols↗
PubMedDate not supplied

Transformation of bile acids into iso-bile acids by Clostridium perfringens: possible transport of 3 beta-hydrogen via the coenzyme.

We have examined the mechanism for the bacterial transformation of chenodeoxycholic acid and lithocholic acid into the corresponding 3 beta-hydroxy epimers with the use of 3 alpha- and 3 beta-tritiated bile acids. The 3-oxo bile acids were transformed into the 3 alpha- (85%) and 3 beta- (15%) hydroxy bile acids after 20-hr incubation with Clostridium perfringens. Approximately 75% radioactivity was recovered in the aqueous medium when [3 beta-3H]chenodeoxycholic acid or [3 beta-3H]lithocholic acid was incubated with the bacteria, and approximately 15% of radioactivity in the bile acid fraction was associated with the 3 alpha-position of the iso-bile acids. When [3 beta-3H]chenodeoxycholic acid was incubated with unlabeled 3-oxo-5 beta-cholanoic acid, tritiated litho- and iso-lithocholic acids were recovered. These results can be explained only when a 3-oxo intermediate is postulated, and the 3 beta-hydrogen in the bile acids is transferred by the bacterial coenzyme (NAD+ or NADP+) to the 3 alpha-position in the iso-bile acids during the reduction of the 3-oxo compounds.

Bile Acids and Salts↗
PubMed1993

Mechanism of trichloroethylene-induced elevation of individual serum bile acids. II. In vitro and in vivo interference by trichloroethylene with bile acid transport in isolated rat hepatocytes.

The effects of trichloroethylene (TRI) on bile acid transport in isolated rat hepatocytes have been studied using doses ranging from 0.5 to 4.0 microliters/flask and a 20-min equilibration period. It was found that TRI caused a dose-related suppression of initial rates of uptake of cholic acid (CA) and taurocholic acid (TC) with no significant effect on enzyme leakage and intracellular potassium ion contents. Accumulation over 30 min for each of those two bile acids was also inhibited. A noncompetitive inhibition of bile acid uptake was shown as indicated by a decrease in maximum velocity (Vmax) and unchanged Michaelis constant (Km). Thirty minutes after cessation of TRI exposure in vitro the uptake of bile acids had gradually returned to normal levels. No significant interference of efflux was found in cells preloaded with either CA or TC. After dosing rats with 1 mmol/kg TRI in vivo the inhibition of uptake of CA and TC by subsequently isolated hepatocytes was not detected until 4 hr. By 16 hr uptake had returned to normal. The accumulation of bile acids was also suppressed at 4 and 8 hr. The inhibition of uptake after in vivo treatment was also noncompetitive. The data are consistent with the reversible increase of serum bile acids (SBA) in experimental animals after exposure to TRI. Furthermore, they support the contention that it is an interference with bile acid uptake, rather than actual cell damage, that is responsible for TRI-induced increases in SBA. Thus, the changes in SBA seem to be the result of interference with a physiological process rather than an event associated with significant pathological consequences.

Animals↗
PubMed1994

Differential effects of cyclosporin A on transport of bile acids by rat hepatocytes: relationship to individual serum bile acid levels.

Cyclosporin A treatment has been reported to induce hepatotoxicity marked by a rise in total serum bile acid and total bilirubin. The mechanism of cyclosporin A-induced hepatotoxicity seems to be related to interference with hepatocellular transport of these substrates although this remains to be fully substantiated. The purpose of this study was to investigate whether the hepatocellular uptake of the different bile acids, in the presence of cyclosporin A, is consistent with the changes in their respective individual serum bile acid concentrations. High-performance liquid chromatography has been used to assay individual serum bile acids in cyclosporin A-treated rats at doses of 0.1, 1, and 10 mg/kg/day for 4 days. Control rats were treated with Cremophor (1 ml/kg/day). At the higher doses, cyclosporin A produced a significant increase in levels of cholic acid, taurocholic acid, chenodeoxycholic acid, and deoxycholic acid compared with controls. Serum glycocholate was unaffected even at the highest dose. Inhibition of initial rate of uptake and accumulation of [14C]cholic acid, [14C]chenodeoxycholic acid, and [14C]deoxycholic acid by isolated rat hepatocytes was consistent with the changes in their respective serum bile acids. Coincubation of rat hepatocytes with unlabeled cholic acid (100 microM), the major serum bile acid in cyclosporin A-treated rats, showed a further inhibitory effect on [14C]cholic acid and [14C]deoxycholic acid accumulation. The initial rate of uptake of [14C]glycocholate was also inhibited. However, accumulation of glycocholic acid did not show significant changes at the longer incubation times (2-30 min). In addition, coincubation of rat hepatocytes with unlabeled cholic acid (100 microM) plus cyclosporin A did not induce any inhibition of glycocholate accumulation. Together, these differences provide an explanation for the unchanged serum levels of glycocholate. In conclusion, the changes in individual serum bile acids in cyclosporin A-treated rats are consistent with the effect of this drug on their hepatocellular accumulation.

Animals↗
PubMed1982

Ultrastructural changes of bile duct epithelium in primary biliary cirrhosis in relation to progression of bile duct loss.

Using wedge liver biopsies from patients with primary biliary cirrhosis (PBC), ultrastructural features of the intrahepatic bile ducts in livers with slight or no bile duct loss were compared with those in livers with advanced bile duct loss and in extrahepatic cholestasis (EHC). Most changes in the biliary epithelium in PBC were similar to those in EHC. Microvillous loss and bleb formation, mitochondrial damage and increase in endoplasmic reticulum and ribosomes were found in PBC irrespective of the degree of bile duct loss, and also in EHC. These changes were present almost equally at any level of the biliary tree, and are presumed to represent a variety of non-specific lesions of biliary epithelial cells. As the loss of bile ducts in PBC progressed, cytoskeletal filaments and cytophagosomes increased in number and basement membranes were more thickened and reduplicated. These changes were more or less conspicuous in smaller branches of the biliary tree, and were also prominent in EHC. They might be causally related to the bile flow disturbance in the liver. Lateral intercellular spaces were irregularly dilated and contained osmiophilic membranous and/or granular material, similar to that found in duct lumena, within and without the basement membrane, and in the cytoplasm of periductal macrophages. Furthermore, pinocytotic vesicles were increased in the biliary cytoplasm facing periphery. These findings suggest possible alteration of the permeability of biliary epithelial cells, probably in the direction from the lumena to the periductal tissue. Such changes were found in PBC livers with virtual absence of bile duct loss, and the significance of this phenomenon is discussed.

Bile Ducts, Intrahepatic↗
PubMed1993

Bile-induced acute pancreatitis in cats. Roles of bile, bacteria, and pancreatic duct pressure.

The relationship between pancreatic duct pressure, bile, bacterial infection of bile, and the development of acute pancreatitis was studied in a feline model. The cat main pancreatic duct was perfused from the head to the tail of the gland with bile and/or Escherichia coli bacteria at "basal" pancreatic duct pressure (< 10 cm H2O) and at pancreatic duct pressure in the upper physiologic range (45 cm H2O). Sterile bile and sterile control solution produced no inflammatory alterations at either pressure. Infected control solution caused a mild acute edematous pancreatitis under low and high pressure. Infected bile caused a severe acute edematous pancreatitis at basal duct pressure; at high pressure, additional focal acinar necrosis was observed in the majority of animals. Infected bile was found to raise basal pancreatic duct pressure by 30%. The other test solutions, which caused only mild inflammatory alterations of the pancreas, did not alter duct pressure. We conclude: (1) Bacterial infection is important for the initiation of acute pancreatitis in this model. (2) High physiologic duct pressure may result in the conversion of nondestructive forms of the inflammation to acinar necrosis. (3) Infected bile-induced increase in duct pressure is likely to result from compression of the duct lumen by the inflammatory edema of the gland.

Acute Disease↗
PubMed1998

Ursodeoxycholic acid increased bile flow and affects bile composition in the early postoperative phase following liver transplantation.

Orally given ursodeoxycholic acid (UDCA) has beneficial effects on laboratory parameters in different cholestatic conditions. In order to investigate the effect on early graft function after liver transplantation, 33 patients were randomized to receive either UDCA 15 mg/kg per day or placebo from the 1st postoperative day until 3 months after transplantation. All liver grafts produced bile within 24 h after revascularization. In both groups there was an increasing bile flow each day until day 5 after transplantation. This increase was more pronounced in the UDCA group where the flow on day 2 reached a mean value of 183 +/- 28 ml/day compared to 106 +/- 17 ml/day in the placebo group (P < 0.05). The average daily volume of bile produced during the first 10 days was also found to be higher in the UDCA group compared to the placebo group (242 +/- 20 ml vs 176 +/- 18 ml, P < 0.02). In the UDCA group a significant decrease in total bile acid output between the 5th and 10th postoperative days was found, while in the placebo group the amount of bile acids excreted remained stable over time. The composition of bile differed between the two groups with an increase in the portion of UDCA in the UDCA group from the 2nd postoperative day (25% vs 4.6%, P < 0.0003). The fraction of UDCA then remained high during the whole study period with a peak at day 3 when 38.1 +/- 6.6% of the bile acids consisted of UDCA. In the placebo group, the fraction of UDCA was low from the beginning and diminished further over time. Prophylactic UDCA treatment was found to have a significant positive impact on the ALT level during the 4th and 5th postoperative days, but had no effect on bilirubin or GGT in the early postoperative phase (days 1-10). No differences in cyclosporine requirement were found between the two groups.

Adult↗
PubMed2004

Effect of glutamine and bile acid on hepatocyte apoptosis after bile duct ligation in the rat.

Apoptosis is an important process in a wide variety of biologic systems. Cholestasis, or impaired bile formation, occurs in a wide variety of human liver diseases. Retention and accumulation of toxic hydrophobic bile salts in hepatocytes may cause hepatocyte toxicity by inducing apoptosis. In addition, the translocation of bacteria and endotoxin, well documented in patients with obstructive jaundice, contribute to the induction of hepatocyte apoptosis. We hypothesized that oral bile acid replacement, glutamine administration, or both can attenuate or abolish hepatocyte apoptosis. Male Sprague-Dawley rats weighing 250 to 300 g were randomized to four groups (10 in each group). Group 1 underwent a sham operation and was simultaneously treated with normal saline. Group 2 underwent common bile duct (CBD) ligation and was simultaneously treated with normal saline. Group 3 underwent CBD ligation and was simultaneously treated with oral glutamine. Group 4 underwent CBD ligation and was simultaneously treated with oral bile acid replacement. After 3 days (n = 5) and 7 days (n = 5), liver tissues were harvested for histopathologic analysis and apoptosis measurements. When compared with the sham operation group, significantly increased hepatocyte apoptosis and ductular proliferation occurred after CBD ligation for either 3 or 7 days. After administration of either glutamine or bile acid, the increased hepatocyte apoptosis and ductular proliferation after CBD ligation for 3 days were significantly diminished. However, both failed to diminish the changes after CBD ligation for 7 days. Significantly increased hepatocyte apoptosis and ductular proliferation occurred after CBD ligation. The administration of either glutamine or bile acid effectively diminished the hepatocyte apoptosis and ductular proliferation after CBD ligation for 3 days, whereas both failed to show the same effect after CBD ligation for 7 days.

Administration, Oral↗
PubMed1976

Concentration changes of bile acids in sequential segments of pigeon intestine and their relation to bile acid absorption.

Changes in the concentration of bile acids in sequential segments of pigeon intestine were measured. It was found that the jejunum has the highest concentration of bile acids. When the ratio of bile acids to beta-sitosterol (a non-absorbable dietary marker) was examined in contents of various segments, it was found that the ratio showed a marked decrease (86.6%) from the upper to lower jejunum while the subsequent changes in other segments were not as striking. This indicates that the jejunum is the major site of bile acid absorption in the pigeon, unlike in mammals, where the ileum has been shown to be the major site of bile acid absorption. This notion was confirmed by studies of the effect of ileal bypass in these pigeons. This surgical procedure did not significantly change the fecal excretion of bile acids or neutral sterols indicating that the jejunum is capable of maintaining a normal enterohepatic circulation of bile acids in the absence of the ileum in the pigeons.

Animals↗