SEARCH · Search PubMed

Results for “BILE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

PubMed2003

Vectorial transport of bile acids in immortalized mouse bile duct cells.

In ileal epithelial cells, apical sodium-dependent bile acid transporter (ASBT) is responsible for the uptake of bile acids from the lumen. Furthermore, ASBT is expressed in the apical plasma membrane of intrahepatic bile duct cells (BECs). Using cultured immortalized mouse intrahepatic BECs that form monolayers or cysts, vectorial transport of bile acids was studied. [3H]-taurocholic acid ([3H]-TCA) was transported through monolayers transcellularly almost exclusively from the apical to the basolateral side in a Na(+)- and a temperature-dependent manner. Transport of [3H]-TCA was inhibited by 59.3+/-18.6% in the presence of taurochenodeoxycholic acid. Uptake of lysyl fluorescein-conjugated bile acid, Cholyl-[Nepsilon-NBD]-lysine, was seen in a Na(+)- and a temperature-dependent manner from the apical side of BECs that form monolayer or cysts. Reverse transcription-polymerase chain reaction for mRNAs in the cells showed presence of mRNAs for ASBT and farnesoid X receptor (FXR), a nuclear bile acid receptor. In conclusion, intrahepatic BECs transport bile acids mainly from the apical to the basolateral side in concert with ASBT and maybe FXR in the cells.

Journal Article↗

PubMed1993

Bile duct injury and bile leakage in laparoscopic cholecystectomy.

Between January 1991 and July 1992, 350 laparoscopic cholecystectomies were performed. There were six biliary complications (1.7 per cent): common bile duct (CBD) injury (one patient), delayed CBD necrosis (one), immediate postoperative bile leakage (one) and delayed bile leakage (three). All six patients required laparotomy. Primary repair with long-arm T tube splinting for 3 months was performed for the CBD injury. Religation of the cystic duct was carried out after immediate postoperative bile leakage. Laparotomy with T tube choledochostomy only was performed in the three patients with delayed bile leakage, and hepatojejunostomy Roux-en-Y was undertaken for CBD necrosis. The patient with primary repair of the CBD injury required choledochojejunostomy Roux-en-Y 18 months later for stenosis. Episodes of intermittent cholangitis occurred in the patient with CBD necrosis. The outcome for the four patients with bile leakage was good. There were no deaths.

Adult↗

PubMed2006

Atp8b1 deficiency in mice reduces resistance of the canalicular membrane to hydrophobic bile salts and impairs bile salt transport.

Progressive familial intrahepatic cholestasis type 1 (PFIC1, Byler disease, OMIM 211600) is a severe inherited liver disease caused by mutations in ATP8B1. ATP8B1 is a member of the type 4 subfamily of P-type ATPases, which are phospholipid flippases. PFIC1 patients generally develop end-stage liver disease before the second decade of life. The disease is characterized by impaired biliary bile salt excretion, but the mechanism whereby impaired ATP8B1 function results in cholestasis is unclear. In a mouse model for PFIC1, we observed decreased resistance of the hepatocanalicular membrane to hydrophobic bile salts as evidenced by enhanced biliary recovery of phosphatidylserine, cholesterol, and ectoenzymes. In liver specimens from PFIC1 patients, but not in those from control subjects, ectoenzyme expression at the canalicular membrane was markedly deficient. In isolated mouse livers Atp8b1 deficiency impaired the transport of hydrophobic bile salts into bile. In conclusion, our study shows that Atp8b1 deficiency causes loss of canalicular phospholipid membrane asymmetry that in turn renders the canalicular membrane less resistant toward hydrophobic bile salts. The loss of phospholipid asymmetry may subsequently impair bile salt transport and cause cholestasis.

Adenosine Triphosphatases↗

PubMedDate not supplied

The effects of cyclic imides on lipid absorption from the intestine and on bile lipids and bile acids of Sprague Dawley rats.

The cyclic imides, o-(N-phthalimido)acetophenone, 2,3-dihydrophthazine-1,4-dione and N(4-methyl phenyl)diphenimide, were evaluated for their effects on bile lipids, bile acids, small intestinal absorption of cholesterol and cholic acid and liver and small intestinal enzyme activities involved in lipid metabolism. The agent at 20 mg/kg/day orally elevated rat bile excretion of lipids, e.g. cholesterol and phospholipids, and increased the bile flow rate. These agents altered the composition of the bile acids, but there was no significant increase in lithocholic acid which is most lithogenic in rats. The three agents did decrease cholesterol and cholic acid absorption from isolated in situ intestinal duodenum loops in the presence of drug. Hepatic and small intestinal mucosa enzyme activities, e.g. ATP-dependent citrate lyase, acyl CoA cholesterol acyl transferase, cholesterol-7-alpha hydroxylase, sn-glycerol-3-phosphate acyl transferase, phosphatidylate phosphohydrolase, and lipoprotein lipase were reduced. However, the cyclic imides did not accelerate HMG-CoA reductase activity, the regulatory enzyme for cholesterol synthesis, in a manner which would accelerate biliary cholesterol excretion. There was no evidence of hepatic cell damage afforded by the drugs based on clinical chemistry values which would induce alterations in bile acid concentrations after treatment of the rat.

Animals↗

PubMed1981

Effects of clofibrate and tiadenol on the elimination of lipids and bile acids in rat bile.

The aim of the work presented here was to compare the biliary elimination of cholesterol and the different bile acids of rats that had been made hypolipidemic by short-term treatments with clofibrate or tiadenol. Both treatments induced a significant decrease in cholesterol output in the bile. The analysis of the different bile acids showed a decrease in dihydroxylated acids elimination (especially CDC acid) without any difference between the 2 sexes. This decrease was associated with an increase in cholic acid excretion. These results are directly correlated with the dose of the administered hypolipidemic drug. The drugs caused as significant increase in the ratio of trihydroxylated acids of the bile and on the output was obtained, for both drugs, with a treatment of 200 mg/kg/day. Clofibrate had a greater effect than tiadenol at this dose. Both drugs show a greater effect on lowering serum lipid levels in female animals when compared to males, whereas elimination of bile cholesterol and modifications of bile acids were greater in male animals than female animals.

Animals↗

PubMed1977

Intraoperative measurement of the bile flow resistance in the terminal portion of the common bile duct and its clinical significance in biliary surgery.

A practical method, safe and relatively simple to perform, which we have developed for the intra-operative measurement of the resistance to bile flow in the terminal portion of the common bile duct is described. This method performed routinely in conjuction with the operative cholangiography in the operating room, proved to be a powerful diagnostic acid for detecting abnormalities in the terminal portion of the common bile duct. In gallstone disease, the results by this method were compared with the operative results. It was found that minimal organic changes or functional disturbances in the terminal portion of the common bile duct, even those without jaundice, can be detected, and unnecessary choledochotomy or sphincteroplasty avoided. This method has a further advantage in that it gives universality to the resistance R and the residual pressure P as quantitative discriptive indices for the qualitative state of bile flow in the terminal portion of the common bile duct, and, if adopted as a standard and routine method, should make the comparison of works by different investigators easier and more significant.

Bile↗

PubMed1995

Effects of hyodeoxycholic acid and alpha-hyocholic acid, two 6 alpha-hydroxylated bile acids, on cholesterol and bile acid metabolism in the hamster.

The effects of hyodeoxycholic (HDCA) and alpha-hyocholic acids (alpha-HCA), on cholesterol, bile acid and lipoprotein metabolism, were studied in hamsters. The animals were fed a low cholesterol control diet supplemented with 0.1% HDCA or alpha-HCA for 3 weeks. In both treated groups, the LDL-cholesterol concentration was significantly lowered and was associated with a global hypocholesterolemic effect. Moreover, hepatic cholesterol ester storage was reduced and HMGCoA reductase activity was respectively enhanced 13.5-times and 7.7-times in HDCA and alpha-HCA groups compared to controls. In contrast, cholesterol 7 alpha-hydroxylase activity and LDL-receptor activity and mass were not modified. In bile, the cholesterol saturation index was increased 5-fold (HDCA group) and 2-fold (alpha-HCA group) as a consequence of an enlarged proportion of biliary cholesterol. The two 6-hydroxylated bile acids induced an enhanced fecal excretion of neutral sterols (HDCA group: 11.6-times, alpha-HCA group: 3.2-times versus controls) which was consistent with a 59% decrease in intestinal cholesterol absorption in the HDCA group. The major effects due to bile acid treatments were a decrease in LDL-cholesterol concentration, a strong stimulation of hepatic cholesterol biosynthesis and an excessive loss of cholesterol in feces. These perturbations might be the result of the enrichment of bile with hydrophilic bile acids, leading to a limited return of endogenous cholesterol from the intestine to the liver.

Animals↗

PubMed1990

Regulation of plasma cholecystokinin levels by bile and bile acids in the rat.

To determine whether intraduodenal bile acids inhibit pancreatic secretion and cholecystokinin (CCK) release independent of pancreatic proteases, experiments were conducted in rats with bile and pancreatic juice chronically diverted to the ileum. Diversion of bile and pancreatic juice increased plasma CCK concentration to 19.1 +/- 4.0 pmol/L. Intraduodenal sodium taurocholate (78 mumol/h) reduced plasma CCK concentration to 6.6 +/- 1.5 pmol/L after 1 hour, but values increased to 17.3 +/- 2.3 pmol/L after 13.5 hours despite continued taurocholate infusion. Pancreatic protein secretion was also significantly but transiently inhibited by taurocholate. However, neither acute nor chronic intraduodenal bile infusion significantly reduced plasma CCK concentration compared with sodium bicarbonate infusion (13.4 +/- 1.9 pmol/L vs. 15.0 +/- 1.7 pmol/L, respectively). Chronic (13.5 hours) intraduodenal infusion of taurocholate plus pancreatic juice caused a sustained reduction of plasma CCK level to 3.1 +/- 0.5 pmol/L, which significantly increased to 9.4 +/- 1.1 pmol/L after cessation of taurocholate but with continued infusion of pancreatic juice. The results indicate that bile does not inhibit CCK release and that bile acids do not physiologically inhibit pancreatic secretion or CCK release independent of the presence of pancreatic proteases.

Animals↗

PubMed1991

Diabetes-induced bile acid composition changes in rat bile determined by high performance liquid chromatography.

The distribution of glycine and taurine conjugated bile acids in bile from streptozotocin-induced diabetic rats were determined by high performance liquid chromatography (HPLC). Biliary bile acid output in diabetic rats was significantly greater compared to control (p less than 0.001). The increase is not a generalized effect of diabetes, but is the preferential increased production of taurochenodeoxycholic acid. These observed changes in bile acid composition may represent greater capacity of bile from diabetic rats to solubilize cholesterol. In the absence of a gallbladder, however, rat bile undergo continuous enterohepatic circulation, and consequently is not subjected to modifications by gallbladder epithelial cells that would potentiate cholesterol precipitation.

Animals↗

PubMed1985

Enhancement of the autocatalytic activation of trypsinogen to trypsin by bile and bile acids.

The activation of trypsinogen to trypsin in the small intestine can occur by the action of enterokinase or, alternatively, as an autocatalytic process catalysed by trypsin itself. We have found that bile salts and human bile cause a significant enhancement of the autocatalytic activation of trypsinogen. This effect is dependent on the calcium ion concentration and is most marked around pH 5.4 and 7.8. An optimum concentration exists for each bile salt at which the greatest enhancement occurs. At this concentration, certain bile salts have been shown to produce activation effects of up to 55-fold. It is suggested that this activation of the autocatalytic process by bile plays an important role in protein digestion in the small intestine, since it has been shown previously that duodenal trypsin levels are abnormally low in patients with an impairment of bile secretion.

Bile↗

PubMed1986

Relationships between bile salts hydrophilicity and phospholipid composition in bile of various animal species.

Bile salts and phospholipids from bile of chicken, dog, sheep, rat, ox, pig, guinea-pig and man were analyzed by high-performance liquid chromatography. Bile salts showed marked differences in their hydrophilic properties, owing to hydroxyl structure and type of conjugation. Phospholipids were generally similar, containing 90-95% of phosphatidylcholine which was made of molecular species containing palmitic acid in the sn-1 position. The comparative analysis of bile salts and phosphatidylcholines profile demonstrated that bile salts hydrophilicity influences the quantity of phosphatidylcholine in bile but not the quality.

Animals↗

PubMed1997

Influence of bile salts on molecular interactions between sphingomyelin and cholesterol: relevance to bile formation and stability.

Bile salts enhance secretion of cholesterol into bile and its subsequent solubilization with phosphatidylcholine in mixed micelles. Sphingomyelin, a major structural lipid of the hepatocyte canalicular membrane, and disaturated phosphatidylcholines are known to impede nucleation of solid cholesterol crystals in supersaturated model systems. To understand these effects physico-chemically, we compared the influence of bile salts on interactions of cholesterol with natural sphingomyelins, as well as with dipalmitoyl and egg yolk phosphatidylcholines using various in vitro systems. Submicellar bile salts enhanced significantly bidirectional transfer of dehydroergosterol (a fluorescent cholesterol analog) between sphingomyelin and egg yolk phosphatidylcholine vesicles in the rank order taurocholate < tauroursodeoxycholate < taurodeoxycholate. Quasielastic light scattering of serially diluted sphingomyelin-taurocholate mixtures (1:1 molar ratio, 3 g/dl) revealed metastable temperature-dependent transitions between globular micelles, rod-shaped micelles and vesicles, suggesting that phase transitions under these experimental conditions were metastable only at temperatures below 37 degrees C. Ternary phase diagrams of all sphingomyelins and dipalmitoyl phosphatidylcholine with cholesterol and taurocholate (37 degrees C, 3 g/dl, 0.15 M NaCl) were identical. Compared to systems containing egg yolk phosphatidylcholine, the 1-phase micellar zone and 2- and 3-phase solid cholesterol crystal-containing zones were reduced markedly while the 2-phase zone with stable cholesterol-sphingomyelin liquid crystals was greatly expanded. Our results suggest that the high affinity of cholesterol for sphingomyelin is lost in the presence of bile salts. Our findings may be relevant to secretion of cholesterol into bile and to its inability to crystallize in the hepatocyte canalicular lumen or its surrounding membranes.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1986

Phospholipid degradation in, and protein content of, rat fistula bile. Contamination of bile with pancreatic juice.

The extent to which pancreatic juice can contaminate bile collected from a rat with a biliary fistula has been investigated by cannulating the bile duct proximal to either the duodenum or the liver, and by stimulating pancreatic flow with secretin. Bile collected via a fistula proximal to the duodenum showed marked pancreatic contamination. Thus, bile collected via a fistula proximal to the duodenum has a higher flow rate, a greater total protein and amylase content and a different polypeptide profile than bile collected via a fistula proximal to the liver. The phospholipid content also differed in that phosphatidylcholine was converted enzymically to lysophosphatidylcholine. Secretin increased bile flow and the biliary output of total protein and amylase when the fistula was proximal to the duodenum, but had no effect upon these parameters when the fistula was proximal to the liver, or in the isolated perfused rat liver.

Amylases↗

PubMed1989

Bile acids in bile after monensin treatment.

Bile derived from monensin treated bile-fistula rats has been analysed for bile acids content. Bile flow and bile acids decrease in bile following monensin treatment, in agreement with the disruption of the Na+ gradient determined by the ionophore and necessary for the vectorial Na+-cotransport of taurocholate at the sinusoidal pole of the hepatocyte.

Animals↗

PubMed1993

Regulation of bicarbonate-dependent ductular bile secretion assessed by lumenal micropuncture of isolated rodent intrahepatic bile ducts.

While intrahepatic bile duct epithelial cells secrete bile through transport of ions and water, the physiological mechanisms regulating ductular bile secretion are obscure, in part because of the lack of suitable experimental models. We report here the successful micropuncture of the lumen of isolated intrahepatic bile ducts and direct measurements of ductular ion secretion. Intact, polarized bile duct units (BDUs) were isolated from livers of normal rats by enzymatic digestion and microdissection. BDUs were cultured and mounted on a microscope in bicarbonate-containing buffer, and the lumens were microinjected with 2',7'-bis(2-carboxyethyl)-5-(and -6)carboxyfluorescein (BCECF)-dextran. Lumenal pH was measured by ratio imaging of BCECF fluorescence using digitized video fluorescent microscopy. After 36 hr in culture, the ends of BDUs sealed, forming closed compartments. After lumenal microinjection of BCECF-dextran, fluorescence was stable at the pH-insensitive wavelength, indicating no dye leakage. Serial changes in pH of extralumenal buffers containing pH-gradient collapsing ionophores allowed us to establish reliable standard curves relating fluorescence ratio to lumenal pH (r = 0.99; P < 0.001). By this approach, the basal pH inside the lumen of BDUs was 7.87 +/- 0.08 units (n = 9), 0.47 unit higher (P < 0.001) than the bathing buffer pH. Addition of 100 microM forskolin increased (P = 0.02) the lumenal pH from 7.78 +/- 0.06 to 7.97 +/- 0.06 units (n = 5); the forskolin effect was completely abolished by incubation of BDUs in HCO3-/CO2-free buffer. Moreover, forskolin caused a 50-fold increase in cAMP levels in BDUs. The observations are consistent with cAMP-dependent, active lumenal HCO3- secretion by BDUs. Furthermore, they demonstrate the suitability of the BDU model for studying regulatory and mechanistic aspects of ductular bile secretion.

Analysis of Variance↗

PubMed1994

Dietary modifications of the biliary bile acid glycine:taurine ratio and activity of hepatic bile acid-CoA:amino acid N-acyltransferase (EC 2.3.1) in the rat.

Effects of dietary manipulations on the biliary bile acid glycine:taurine (G:T) ratio and the activity of hepatic bile acid-CoA:amino acid N-acyltransferase (EC 2.3.1) in the post-mitochondrial fraction of liver homogenates were examined in the rat. The G:T ratio in rats fed on the diet containing 100 g pectin/kg (2.18) was markedly higher than that in the animals fed on the diet containing 100 g cellulose/kg (0.09). The diets containing either 10 g cholesterol/kg or 5 g sodium cholate/kg, especially the latter, also increased the G:T ratio (0.77 and 2.33 respectively) compared with a control diet free of these steroids (0.34). When the saturating concentrations of taurine (20 mM) and glycine (100 mM) were the substrates, dietary pectin relative to cellulose significantly increased the activity of both taurine- and glycine-dependent bile acid-CoA:amino acid N-acyltransferase, but neither dietary bile acid nor cholesterol influenced it. In spite of the marked difference in the G:T ratio among the rats given various types of experimental diet, the bile acid-CoA:amino acid N-acyltransferase reaction produced taurine-but little glycone-conjugated bile acid when both taurine and glycine coexisted at physiological concentration ranges in the assay media. Dietary manipulations modified the hepatic taurine concentrations and the changes were inversely correlated with those in the G:T ratio. However, hepatic concentration of taurine (1.67-4.82 mumol/g) in rats given various types of experimental diet was comparable with or even higher than the reported Michaelis constant (Km) value of N-acyltransferase for this compound (0.8-2.5 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

Acyltransferases↗

PubMed2000

Brown pigment stones in the common bile duct: reduced bilirubinate diconjugate in bile.

BACKGROUND: Bilirubin is the main component of most common bile duct stones. Normally, almost all bilirubin in bile is conjugated to glucuronic acid or some other sugar moiety. These conjugates are unstable and liable to deconjugation. Unconjugated bilirubin is insoluble and may precipitate as the calcium salt found in brown pigment stones. The pattern of bilirubin conjugates in common duct bile of patients with choledocholithiasis has been unknown. METHODS: In a clinical series of 55 patients with choledocholithiasis common-duct bile was aspirated, and the bilirubin conjugates analyzed with high-performance liquid chromatography. One stone from each patient was analyzed for cholesterol and bilirubin content to determine stone type. RESULTS: Sixteen patients had cholesterol stones, 38 patients had brown pigment stones, and 1 patient had a black stone. Patients with pigment stones had a lower percentage of bilirubin diglucuronide (median, 60.3%; interquartile range, 49.7%-67.3%) than patients with cholesterol stones (64.0%; 60.2%-73.3%) (Mann-Whitney, P=0.015). No significant difference was found for the other bilirubin conjugates, total bilirubin, or biliary pH when pigment and cholesterol stone patients were compared. The time of bile sampling in relation to papillotomy and treatment of cholestasis was not associated with the low percentage of bilirubin diglucuronide. The observation of reduced values for bilirubin diglucuronide could not be ascribed to duodenal diverticula or Billroth-II gastric resection. CONCLUSION: The percentage of the main bilirubinate conjugate, bilirubin diglucuronide, is decreased in the common duct bile of patients with pigmented compared with cholesterol stones.

Aged↗

PubMed1983

Response of bile flow, biliary lipids and bile acid pool in the pig to quantitative variations in dietary fat.

Bile flow, biliary lipids and bile acid pool have been studied in growing pigs adapted to a semipurified diet of 2, 10 or 20% lard. After a 5-day period of apparent digestibility measurement, bile secretion was studied in previously fistulated pigs. The apparent digestibility of lard was maintained at a very high level, whatever quantity of lard was ingested. Daily bile acid output was 49% higher with the 10% lard diet than with the 2% lard diet, whereas no further increase was observed with the 20% lard diet. There was a direct relationship between bile acid output and pool size. Biliary phospholipid output increased by 29.0% between 2 and 10% dietary lard and by 69.5% between 10 and 20% lard. The corresponding rise in biliary cholesterol output was +33% between 2 and 10 or 10 and 20% lard in the diet. A study of biliary kinetics showed that this adaptation of biliary lipid to dietary fat was observed whatever time of the light/dark cycle was considered. These results, together with a recent demonstration of the implication of endogenous phospholipids in fat digestion, suggested that, in the course of biliary lipid adaptation to dietary fat content, biliary phospholipid could act in synergy with bile salt, resulting in the maintenance of excellent dietary fat digestion.

Animals↗