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PubMedDate not supplied

Effect of ursodeoxycholic acid on biliary bile acid and bile lipid composition in gallstone patients.

In five patients with radiolucent gallstones, the effect of ursodeoxycholic acid (Urso) in doses of 250, 500, 750, 1,000, and 1,250 mg per day on biliary lipid and bile acid composition was studied. Biliary cholesterol decreased from 8.8 +/- 0.8 mole% to 4.4 +/- 0.2 mole% at 500 mg Urso per day (7.1 mg per kg) and to 4.2 +/- 0.3 mole% at 750 mg Urso per day (10.7 mg per kg). Administration of 1,000 or 1,250 mg Urso per day produced no further decrease of biliary cholesterol. The biliary content of phospholipids and total bile acids remained unchanged. During Urso treatment, the relative amounts of glyco-Urso and tauro-Urso in bile increased. Glyco-Urso reached a plateau at 49.1 +/- 2.1% of total bile acids during treatment with 1,000 mg Urso per day, and tauro-Urso increased up to 4.3 +/- 1.5% of total bile acids at 250 mg Urso per day. Simultaneously cholic acid, chenodeoxycholic acid, deoxycholic acid, and lithocholic acid decreased. The data indicate that Urso treatment reduces biliary cholesterol efficiently already at a dose of 500 mg per day; biliary bile acid composition changes up to 1,000 mg Urso per day. Doses greater than 1,000 mg per day produced no additional alterations in bile composition.

Aged↗

PubMed1993

Effect of ursodeoxycholic acid administration on bile duct proliferation and cholestasis in bile duct ligated rat.

The origin, mechanism, and significance of the bile duct proliferation (BDP) associated with cholestasis remain unexplained. This study examined the effect of oral administration of ursodeoxycholic acid (UDCA) on both BDP and cholestasis in the rat. After bile duct ligation, male Sprague-Dawley rats were treated for 30 days with either UDCA (5 mg/day) (group A) or saline solution (group B). Animals were sacrificed at day 30. The serum activity of aminotransferase (ALT, AST), alkaline phosphatase, and gamma-glutamyltransferase (GGT) was significantly lower (P < 0.01) in the UDCA-treated rats. Total serum bilirubin and total serum bile acids were lower (P < 0.001) in group A. Moreover, the control of BA in bile was reduced also (P < 0.02). Conversely, serum cholesterol levels were not different between the two groups. Histological examination showed that the number of ductular cells in the portal areas was significantly (P < 0.001) reduced in UDCA-treated as compared to saline-treated rats. The replication activity, assessed as the number of bromodeoxyuridine-positive cells, was also significantly lower in treated animals (33 +/- 11 vs 64 +/- 22 per 1000 cells; P < 0.001). Lobular bile ductules were three times larger in group B, and extrahepatic duct measurements confirmed this increase in size of the larger biliary ducts (P < 0.001). These findings demonstrate that UDCA reduces BDP in response to BD ligation. Although the mechanism(s) of this effect is still hypothetical, UDCA may reduce the level of irritating bile salts such as chenodeoxycholic acid and lithocolate and increase periductular bile acid recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1978

Effects of cholecystokinin-pancreozymin on bile flow and biliary bile salt secretion in the cholecystectomized animal.

The effects of an intravenous infusion of cholecystokinin-pancreozymin on bile secretion were studied in 13 unanesthetized and cholecystectomized piglets. The results demonstrate that CCK-PZ induces a significant increase of bile flow and bile salt excretion. The excretion patterns for bilirubin and Ioglycamide, however, showed a slight but not significant decrease. Peripheral hemodynamic parameters remained unchanged. A detailed analysis of these results suggests that CCK-PZ induces an increase of biliary bile salt secretion by stimulation of intestinal motility and enhancement of bile salt circulation within the enterohepatic circulation (EHC). In combination with previous studies on the effects of spasmolytics on biliary bile salt excretion these results therefore emphasize, that the intestinal motility and transit time might play a role in the physiology and pathophysiology of biliary bile salt secretion.

Animals↗

PubMed1997

Influence of subchronic administration of oestradiol, ethinyloestradiol and oestradiol sulphamate on bile flow, bile acid excretion, and liver and biliary glutathione status in rats.

The cholestatic effect of the newly developed oestradiol sulphamate (J995) was compared with that of the natural oestrogen oestradiol (E) and of the cholestatic standard oestrogen ethinyloestradiol (EE). Female ovariectomized rats were orally treated for 7 days with oestrogen doses molar equivalent to 0.01, 0.1, 1, and 10 mg E/kg body wt. Bile flow, biliary bile acid and glutathione excretion as well as liver glutathione status were determined after bile duct cannulation under the influence of ketamine anaesthesia. For systemic oestrogen activity, the increase of uterine weight was measured. J995 showed the highest oestrogenic activity followed by EE and E. Impairment of bile flow and biliary glutathione excretion (GSH, GSSG) were found to be in the order E < J995 < EE. As all three oestrogens did not influence bile acid excretion, we postulate that mainly the bile acid-independent fraction of bile flow was inhibited, caused at least partly by impairment of canalicular glutathione transport. Based on the results of these studies, we conclude that a tenfold higher dose of J995 exhibited the same cholestatic effect as EE. Together with higher systemic oestrogenic activity, J995 may be used as a prodrug with reduced hepatic side-effects to replace EE in contraception strategies.

Animals↗

PubMed2003

The cholecystocolic bypass with jejunal interposition graft for bile acid depletion in bile and portal blood in guinea pigs.

Ileal bypass and cholecystostomy are used in children with selected cholestatic diseases to lower the bile acid (BA) levels in bile and blood and improve outcome. The efficacy of a cholecystocolic bypass in achieving the same goals was investigated in guinea pigs. In the study group (n=7), a cholecystocolic bypass was performed using a jejunal graft interposed between the gallbladder and the cecum. In the control group (n=5), a cholecystojejunal bypass was performed with a similar graft implanted in the proximal jejunum. Total BA concentration was measured in bile and portal blood at surgery (D0) and 30 days later (D30) by pooling the concentrations of 7 individual BA. D30/D0 BA ratios were compared. All animals developed normally without clinical symptoms. A 76% reduction in the bile T-BA levels was observed in both groups (p<0.05). A 80% decrease of T-BA levels was observed in portal vein in study group (p<0.05), suggesting that ileal bile flow and BA ileal reabsorption were highly impaired. No change in portal vein BA levels was observed in control group. Cholecystocolic bypass led to a significant loss of bile acids in guinea pigs and might be considered for bile diversion in pediatric patients with selected cholestatic diseases.

Anastomosis, Surgical↗

PubMed2001

Dilated bile canaliculi and attenuated decrease of nerve-dependent bile secretion in connexin32-deficient mouse liver.

Gap junction channels in the rodent liver are composed of connexin26 (Cx26) and connexin32 (Cx32) proteins. Gap junctional intercellular communication in the mouse liver enhances the effects of hormonal or sympathetic stimulation of glucose release from glycogen stores. To determine whether contraction of bile canaliculi and bile secretion are dependent on the function of gap junction channels, we compared wild-type and connexin32-deficient mice. Confocal laser scanning microscopy of the wild-type mouse liver confirmed the close association of connexin26 and -32 proteins with the zona occludens-1 protein and actin filaments of the bile canaliculi. The decrease of bile flow after electrical stimulation of sympathetic nerves in the perfused liver was attenuated in the Cx32-deficient liver compared with wild-type controls. The amount of secreted bile, however, was similar in wild-type and Cx32-deficient livers. Furthermore, Cx32-deficient mice exhibited dilated bile canaliculi, suggesting that the contraction of bile canaliculi could be impaired in these animals.

Alanine Transaminase↗

PubMed2006

Single-step analysis of individual conjugated bile acids in human bile using 1H NMR spectroscopy.

1H and 13C NMR spectra of intact human bile were assigned using one-dimensional (1H and 13C) and two-dimensional (1H-1H and 1H-13C) experiments. Individual conjugated bile acids--glycocholic acid, glycodeoxycholic acid, glycochenodeoxycholic acid, taurocholic acid, taurodeoxycholic acid, and taurochenodeoxycholic acid--were identified. The bile acids were quantified accurately and individually in a single step by using distinct and characteristic amide signals. Making use of 13C NMR, the study also suggests a way to analyze unconjugated bile acids separately, if present. Chemical shift assignments and rapid single-step analysis of individual conjugated bile acids from intact bile presented herein may have immense utility in the study of bile acid metabolism and deeper understanding of hepatobiliary diseases.

Bile↗

PubMed1979

The application of high pressure liquid chromatography to the analysis of bile salts in human bile.

Two high pressure liquid chromatography (HPLC) systems have been evaluated for the separation of conjugated bile salts from human bile. Partisil-10 ODS with mobile phase of methanol/water pH 2 (55 : 45) at 200 nm, 0.1 AUF UV detection gave only partial separation of bile salts. However, a mu Bondapak fatty acid analysis column using isopropanol/8.8 mmol/l potassium phosphate pH 2.5 (32 : 68) as the mobile phase and 193 nm, 0.1 AUF UV detection separated all the six conjugated bile salts in bile. The limit of detection ranged from 0.1 microgram for sodium taurocholate to 0.2 microgram for sodium glycodeoxycholate. The reproducibility and the application of the method to the analysis of conjugated bile salts was demonstrated using bile from five patients. Its application to the studies of hepato-biliary disease is discussed.

Bile↗

PubMed1981

Bile acid content of gallbladder bile and stones in type IIb and IV hyperlipoproteinemia.

We examined the bile acid composition of gallbladder bile using reversed-phase high performance liquid chromatography (HPLC), in normolipemic and hyperlipidemic (types IIb and IV) patients with cholelithiasis and compared them with normal subjects. Similarly, bile acid composition was determined n the gallstones of these patients. No free bile acids were found in any of the samples examined. We observed that gallbladder bile and gallstones of patients with type IV hyperlipidemia showed a significant increase in the percentage of glyco-conjugated bile acids and reduction in taurine conjugates. Based on this finding we postulate that in addition to biliary lipid composition bile acid composition may also play a role in the pathogenesis of cholesterol gallstone formation.

Adult↗

PubMed1983

Direct enzymic fluorimetric method for the determination of individual bile acids in bile.

We describe a new, simple, fluorimetric enzymic method for the determination of individual bile acids in bile. Bile is diluted 4000-fold with water and 3 alpha- and 7 alpha-hydroxy bile acids are determined by equilibrium methods and chenodeoxycholic acid is determined by a differential kinetic method, without any prior separation and preparatory step. The equilibrium methods are based on the reaction of 3 alpha- or 7 alpha-hydroxy bile acids with beta-NAD+ in the presence of the enzyme 3 alpha- or 7 alpha-hydroxysteroid dehydrogenase (HSD). The kinetic method is based upon the reaction of chenodeoxycholic acid with beta-NAD+ in the presence of the enzyme 7 alpha-HSD. All measurements are monitored fluorimetrically. Cholic and deoxycholic acid are calculated by difference. Recovery experiments gave satisfactory results. Gallbladder bile from patients was analysed for the three major bile acids. The proposed method is suitable for clinical use.

Bile↗

PubMed1983

Correlation of bile acid composition between liver tissue and bile.

Bile acid composition of ten paired human livers and bile specimens were compared with gas chromatography-selected ion monitoring. The bile acid composition in liver and in bile was found to be similar but not identical. This difference seems to be a reflection of bile acid synthesis in liver tissue. It is suggested that analysis of bile acid composition in liver tissue is useful to evaluate abnormality of bile acid synthesis in several pathological states.

Bile↗

PubMed1996

Effect of bile on the intestinal bile-acid binding protein (I-BABP) expression. In vitro and in vivo studies.

Enterocytes actively transport bile acids from the ileal lumen to the portal blood. This physiological process greatly contributes to maintaining the bile acid homeostasis. However, little is known about the molecular mechanisms involved in this transport system. The effect of bile on gene expression of the intestinal bile-acid binding protein (I-BABP) expressed in the enterocytes was studied in vivo, using the by-pass method, and in vitro, using organ culture of ileum explants and Caco-2 cell line. The low cytosolic I-BABP concentration and I-BABP mRNA level found in diverted ileum was totally recovered when bile was added in the ileal lumen. Northern blot analysis of the ileal explants revealed a dose-dependent increase in the I-BABP mRNA in the presence of bile. In Caco-2 cells, the I-BABP transcript was dramatically increased in the presence of human bile while it was undetectable in the control cultures. These data offer the first evidence that biliary components regulate the I-BABP gene expressed in the enterocytes.

Animals↗

PubMed1993

Cholesterol and bile acid biodynamics after total small bowel resection and bile diversion in humans.

BACKGROUND: In humans, the patterns of cholesterol and bile acid biodynamics in the absence of the small intestine are not yet known. They are described in two parenterally fed patients several months after total enterectomy and bile diversion. METHODS: After an intravenous pulse of [3H]cholesterol, a long-term study involved the analysis of both the decay in the specific activity of plasma cholesterol and the biliary outputs of sterols and bile acids. RESULTS: Plasma cholesterol input reached 2-3 g/day (vs. 1 g/day in healthy patients), mostly from synthesis. As assessed by sterol balance, whole body cholesterol synthesis approximated 6 g/day (vs. 0.6-0.8 g/day). Unusually, about 60% of the newly synthesized cholesterol was eliminated, without prior transit into the bloodstream, from the liver into the bile. Bile acid conversion concerned over 90% (vs. 40%-50%) of the cholesterol meant to be excreted, issued from plasma or hepatic synthesis. In addition to cholic and chenodeoxycholic acids, one patient secreted up to 1 g/day of 7-epicholic acid. CONCLUSIONS: The stimulation (up to 10-fold) of the cholesterol and bile acid synthesis, stronger than that observed following ileal bypass or resection or complete bile diversion, could well be partially linked to the absence of small bowel tissue per se.

Bile↗

PubMedDate not supplied

Bile acid profiles in bile, urine, and feces of a patient with cerebrotendinous xanthomatosis.

Bile acid profiles of bile, urine, and feces obtained from a patient with cerebrotendinous xanthomatosis on the same day have been analyzed by gas-liquid chromatography-mass spectrometry after fractionation into groups by mode of conjugation by an ion-exchange chromatography. The predominant biliary bile acid was cholic acid conjugated with glycine and taurine. Lesser amounts of the amino acid conjugates of chenodeoxycholic acid, ursodeoxycholic acid, 7-ketodeoxycholic acid, allocholic acid, and deoxycholic acid, and of unconjugated norcholic acid and allonorcholic acid were also present in the bile. The major fecal bile acid was 7-epicholic acid. Relatively large amounts of bile acids were excreted in the urine. Unconjugated 7-epicholic acid, norcholic acid, allonorcholic acid, and cholic acid predominated. The bile acid profiles of the patient were different from those of normal subjects and should be useful for the diagnosis.

Bile↗

PubMed1992

Reversible bile acid changes in bile duct obstruction and its potential for hepatocellular injury.

The etiology of hepatocellular dysfunction resulting from chronic biliary obstruction is not clearly understood. Alterations in bile acid metabolism due to changes in microsomal cytochrome P-450 enzyme activities may have a fundamental role in cholestatic liver injury. This study examines the very early changes in both biliary bile acids and hepatic microsomal cytochrome P-450 content after bile duct obstruction in the rat and the effects of the restoration of bile flow after 3 days of biliary obstruction. We found that early induction of cytochrome P-450 may be a fundamental step in the generation of cholestatic liver injury mediated by hepatotoxic bile acids. The rapid reversal of bile acid changes with reconstituted bile flow indicate that the liver is able to quickly recover when obstruction is relieved. Characterization of this fundamental process may ultimately provide a means of modulation of cholestatic hepatotoxicity.

Animals↗

PubMed1981

The effect of cholesterol feeding on gallbladder bile acids of the rabbit. Evidence that lithocholic acid is a primary bile acid in the rabbit.

The bile acid in gallbladder bile of rabbits fed a normal diet or one containing 2% (w/w) cholesterol have been determined by gas chromatography-mass spectrometry. The predominant bile acids in normally fed rabbits were 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholan-24-oic acid (cholic acid), 3 alpha, 12 alpha-dihydroxy-5 alpha-cholan-24-oic acid (allodeoxycholic acid) and 3 alpha, 12 alpha-dihydroxy-5 beta-cholan-24-oic acid (deoxycholic acid) with very much smaller amounts of 3 alpha-hydroxy-5 beta-cholan-24-oic acid (lithocholic acid) and 3 alpha, 12 beta-dihydroxy-5 beta-cholan-24-oic acid. In the cholesterol-fed animals the lithocholate became a predominant bile acid. Sulphated bile acids accounted for less than 1% of the total bile acids. It is proposed that lithocholic acid may be a primary bile acid in the cholesterol-fed rabbit, formed by an alternative pathway of biosynthesis involving hepatic mitochondria.

Animals↗

PubMed1981

Influence of chronic ascorbic acid deficiency and excessive ascorbic acid intake on bile acid metabolism and bile composition in the guinea pig.

The influence of chronic ascorbic acid (AA) deficiency and excessive ascorbate consumption on bile acid metabolism, liver and plasma cholesterol levels, hepatic microsomal cytochromes and biliary lipid composition was investigated. Male weanling guinea pigs were fed a cereal-based scorbutigenic diet supplemented with four levels of AA for 7 weeks: deficient, 15 and 30 mg/kg; control, 500 mg/kg; and excess, 20,000 mg/kg. Bile acid kinetic parameters were determined following the intraperitoneal administration of [24-14C] chenodeoxycholic acid. Dietary extremes of AA caused similar alterations in the parameters studied. Relative to the control group, the deficient and excess groups exhibited reduced cytochrome P-450 concentration, lower cholesterol 7 alpha-hydroxylase activity, lower bile acid turnover rate, prolonged bile acid half-life and increased plasma and liver cholesterol concentrations. Deficient and excess groups also exhibited lower biliary cholesterol saturation (i.e., increased bile acid-neutral sterol ratios) than controls. Urinary bile acid excretion was 2- to 3-fold higher in excess guinea pigs than in the other three groups. The data demonstrate the exceptional susceptibility of cholesterol 7 alpha-hydroxylase activity to alteration by dietary extremes of AA, resulting in marked inhibition of bile acid synthesis and elevation of cholesterol levels by both inadequate and excessive AA intake.

Animals↗

PubMed1993

Preweaning diet affects bile lipid composition and bile acid kinetics in infant baboons.

We tested, with 14-wk-old baboons before weaning, the hypothesis that bile acid metabolism is differentially affected by breast feeding or by feeding formulas with a high polyunsaturated:saturated fatty acid ratio or with a low ratio, similar to that of breast milk. Bile lipid content, bile acid pool size, fractional turnover rate, synthetic rate and conjugate composition were measured in a single bile sample 9 d after an injection on d 1 of a mixture of [14C]cholic and [14C]chenodeoxycholic acids and an injection of a mixture of [3H]cholic acid and [3H]chenodeoxycholic acid on d 8. The principal biliary bile acid was chenodeoxycholic acid. The only difference in chenodeoxycholic acid metabolism among the infant diet groups was a lower chenodeoxycholic acid synthetic rate in baboons fed the low polyunsaturated:saturated formula compared with those fed the high polyunsaturated:saturated formula or breast-fed. Cholic acid metabolism was significantly affected by infant diet: breast-fed infants had a smaller cholic acid pool size, lower cholic acid percentage of total bile acids, higher cholic acid glycine:taurine conjugate ratio and larger cholic acid fractional turnover rate than formula-fed animals. The polyunsaturated:saturated fatty acid ratio in the formulas did not significantly affect these variables. These results show that differences in bile acid metabolism between breast- and formula-fed infant baboons are limited principally to cholic acid. These differences likely are due to factors other than fatty acid saturation.

Analysis of Variance↗