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PubMed2003

Novel channel structure of bile acid-guest inclusion complex formed between ursodeoxycholic acid and phenanthrene.

The crystal structure of inclusion complex between ursodeoxycholic acid (UDCA), and phenanthrene has been determined. UDCA molecules formed hydrogen bond network to provide the channel structure along b axis, and phenanthrene molecules were accommodated in the cavity with a stoichiometry of 1 : 1 molar ratio. The channel structure observed in the UDCA-phenanthrene complex was significantly different from that of inclusion complex previously reported for deoxycholic acid (DCA) and cholic acid (CA). Because of the mesh-like hydrogen bond network, channel framework of UDCA could have less flexibility than that of DCA and CA. The difference of molecular state of phenanthrene was clearly observed in solid-state fluorescence measurement.

Bile Acids and Salts↗

PubMed1981

Serum level of biliary glycoprotein I, a determinant of cholestasis, of similar use as gamma-glutamyltranspeptidase.

Biliary glycoprotein I (BGP I), a constituent of normal bile and serum, is a glycoprotein (mol. wt. approximately 90,000) containing about 40% carbohydrate. Serum BGP I (S-BGP I) was determined by means of a double-antibody radioimmunoassay in patients with liver and gastrointestinal disease and in healthy individuals. The serum levels of five liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase (S-ALP), gamma-glutamyltranspeptidase (S-GT), and lactic dehydrogenase), bilirubin (total and conjugated), and bile acids (cholic and chenodeoxycholic acid) were determined in parallel. Healthy individuals had 0.5 +/- 0.3 mg/l of S-BGP I (mean +/- 2 S.D.; range, 0.2-0.9 mg/l). Most patients with liver disease (chronic hepatitis, alcoholic cirrhosis, primary biliary cirrhosis) had elevated levels, up to 5-10 times the upper reference limit, whereas most patients with gastrointestinal disease (ulcerative colitis, Crohn's disease, other GI diseases) had normal values. In patients with liver disease S-BGP I was positively correlated (p less than 0.0005) to S-GT. In primary biliary cirrhosis a positive correlation (p less than 0.005) between S-BGP I and S-ALP was also obtained. All other comparisons between S-BGP I and the other liver function tests showed non-significant correlations. It is concluded that S-BGP I is a determinant of cholestasis of similar use as S-GT.

Adolescent↗

PubMed1994

Influence of ursodeoxycholic acid on biliary lipids.

The advent of bile acid therapy has shed some light on the mechanisms involved in determining bile lipid secretion. The administration of cholelytic bile acids results in a lowering of cholesterol percent molar and saturation index due to a reduction in cholesterol secretion. Studies carried out after administration of bile acids showed initially that biliary cholesterol secretion rates were dependent on the hydrophobic/hydrophilic balance of the prevailing bile acid present in bile. However, more detailed investigations showed that some bile acids (cholic and chenodeoxycholic acids) did not follow this rule because of the presence of other mechanisms involved in determining biliary cholesterol secretion and a possible link between cholesterol synthesis and biliary cholesterol secretion. Several different human models have been used in more recent studies to arrive at a better understanding of the mechanisms involved in determining bile lipid secretion: obese patients, obese patients in rapid weight loss, patients with non-familial hypercholesterolemia and primary biliary cirrhosis. The findings in these studies indicate how modifications in biliary lipid secretion can easily be induced when there are changes in the relative amounts of bile acids. These changes may bring about modifications in intestinal absorption, liver synthesis, and secretion of cholesterol and bile acids that could possibly lead to the formation of lithogenic bile and subsequently to cholesterol gallstones.

Bile Acids and Salts↗

PubMed1994

Ursodeoxycholic acid therapy in primary biliary cirrhosis.

In a total of 1004 patients in 11 controlled trials, treatment with ursodeoxycholic acid (UDCA) 8-15 mg/kg bodyweight per day led to a decrease of pruritus in 30-60% of cases, a decrease in aminotransferases and cholestasis-indicating enzymes in serum by 20-80%, and a decrease of serum bilirubin by 3-40%. A statistically significant improvement in liver histology was found in only two of these studies; in three others there was a positive trend. In three more trials histology was not examined, and in three studies there was no improvement. In the four studies investigating the time elapsed before liver transplantation and the number of deaths, only one definitely found that this was prolonged by UDCA, although in two of the other three there was a positive trend. During treatment, UDCA constitutes 30-50% of the total bile acids in bile and serum; however, its influence on the toxic bile acids is debatable. Cholic acid decreases, but deoxycholic acid and chenodeoxycholic acid are reduced to a lesser degree. UDCA therapy has now been practiced for 12 years and all authors consider the treatment to be safe, but the mode of action of UDCA is still unknown.

Clinical Trials as Topic↗

PubMed1999

Dietary L-arginine attenuates expression of vascular cell adhesion molecule-1 in the aortae of hypercholesterolemic rats.

OBJECTIVE: To determine whether the antiatherogenic effect of L-arginine is due to an inhibition of vascular cell adhesion molecule-1 (VCAM-1) expression in the aortae of hypercholesterolemic rats. METHODS: Twenty-four male Wistar rats were randomized into three groups: Group NC with normal diet (NC, n = 8), Group CC with 4% cholesterol and 1% cholic acid diet (CC, n = 8), Group AC with 4% cholesterol and 1% cholic acid diet supplemented with 3% L-arginine HCl in the drinking water (AC, n = 8). Eight weeks later, the blood samples were collected for biochemical studies, and the aortae were harvested for RT-PCR and immunohistochemical studies. RESULTS: The results showed that dietary L-arginine supplementation reduced expression of VCAM-1 in protein level and mRNA level. CONCLUSION: Inhibitory effect of dietary supplementation of L-arginine on VCAM-1 expression may be one of the mechanisms of its antiatherosclerosis.

Animals↗

PubMed1989

[Respiratory and circulatory changes after the intratracheal infusion of bile acids in dogs].

We studied the effect of intratracheally infused bile acids on the respiratory and circulatory systems in anesthetized dogs. The bile acids used were cholic acid, deoxycholic acid, taurocholic acid, glycocholic acid and taurodeoxycholic acid. They were diluted to 1% or 10% with normal saline solution and 1 ml.kg-1 was infused into the trachea through an endotracheal tube under a controlled ventilation with air. Injection of 10% diluted bile acid, except for glycocholic acid, decreased PaO2 to less than 50 torr after 15 minutes and increased PaCO2 to above 60 torr after 2 hours. A butterfly shadow appeared in chest radiographs after 1 hour. Microscopic examinations revealed severe pulmonary edema and hemorrhage but circulatory depression was negligible. Hypoxia and hypercapnea were also observed in the 1% dilution group but to a smaller degree. Intrapulmonary water volume increased following injection of bile acid. Our results demonstrated that bile acids induce pulmonary damage.

Animals↗

PubMed1989

Ketonic bile acids in urine of infants during the neonatal period.

Ketonic bile acids have been found to be quantitatively important in urine of healthy infants during the neonatal period. In order to determine their structures, the bile acids in urine from 11 healthy infants were analyzed by gas-liquid chromatography-mass spectrometry (GLC-MS) and three samples with particularly high levels of ketonic bile acids were selected for detailed studies by ion exchange chromatography, fast atom bombardment mass spectrometry, microchemical reactions, and GLC-MS. The major ketonic bile acid was identified as 7 alpha, 12 alpha-dihydroxy-3-oxo-5 beta-chol-1-enoic acid, not previously described as a naturally occurring bile acid. The positional isomer 7 alpha, 12 alpha-dihydroxy-3-oxo-4-cholenoic acid, recently described as a major urinary bile acid in infants with severe liver diseases, was also excreted by most infants. Three acids related to cholic acid were identified: 7 alpha, 12 alpha-dihydroxy-3-oxo-, 3 alpha, 12 alpha-dihydroxy-7-oxo-, and 3 alpha, 7 alpha-dihydroxy-12-oxo-5 beta-cholanoic acids. Five bile acids having one oxo and three hydroxy groups were also present. Based on mass spectra and biological considerations two of these were tentatively given the structures 1 beta, 7 alpha, 12 alpha-trihydroxy-3-oxo- and 1 beta, 3 alpha, 12 alpha-trihydroxy-7-oxo-5 beta-cholanoic acids. Some of the others had a hydroxy group at C-4 or C-2. The levels of ketonic bile acids were higher on the third than on the first day of life, and lower after 1 month. The formation and excretion especially of 3-oxo bile acids is proposed to result from changes of the redox state in the liver in connection with birth.

Bile Acids and Salts↗

PubMed1987

[Intestinal scleroderma: clinical aspects, diagnostic possibilities and therapy].

Progressive Systemic Scleroderma (PSS) is a generalized disease of the connective tissue, caused by vascular changes, an increased collagen synthesis as well as inflammatory and immunological phenomena. Manifest intestinal scleroderma is a rare complication. The connection of internal symptomatology with esophagus attack is of practical importance. The bacterial deconjugation of bile acids is of pathogenetic relevance, regarding the release of an intestinal symptomatology. This results in a direct application of Tetracycline or Metronidazole by parenteral administration. The increase of unconjugated serum bile acids, such as cholic acid and chenodeoxycholic acid, gives a diagnostic indication which can be carried out in special laboratories by means of gas-chromatography.

Bile Acids and Salts↗

PubMed1983

Bile acids in patients suffering from colorectal carcinoma--a pilot study.

Bile acids are increasingly discussed in the genesis of colorectal carcinoma. In a pilot study we analysed bile acids in tumor tissue, tumor-free mucosa, serum, and feces of 6 patients with rectal and 3 patients with colonic carcinoma. 5 patients dead from nongastroenterological diseases and two operated on for benign colonic stenosis served as controls for colorectal mucosa, 16 healthy persons as controls for feces and serum. Bile acids and their sulphates were determined after differential solvolysis by gas-liquid chromatography on QF-1 columns. Serum lithocholic acid was significantly (p less than 0, 05) elevated in all carcinoma patients. The feces showed a trend towards increased secondary bile acids. Tumor-free mucosa of patients with rectal carcinoma showed elevated unsulphated bile acids, sulphated lithocholic acid (p less than 0, 05) and sulphated chenodeoxycholic acid (p less than 0, 025) were significantly decreased. In rectal carcinoma tissue total bile acids were elevated, cholic acid (p less than 0, 01) and sulphated lithocholic acid decreased (p less than 0, 05). In nonaffected colonic mucosa of patients with colonic carcinoma total bile acids were decreased, in colonic carcinoma tissue only traces of bile acids were found. Whether these changes are causes or rather consequences of colorectal tumors--e.g. tumor-induced stasis in the gut--and whether they may be useful for diagnosis remains to be elucidated in further studies.

Adult↗

PubMed1982

Enhancement of the 7 alpha-dehydroxylase activity of a gram-positive intestinal anaerobe by Bacteroides and its significance in the 7-dehydroxylation of ursodeoxycholic acid.

The 7 alpha-dehydroxylation of chenodeoxycholic acid (CDCA) and cholic acid (CA) by a Eubacterium lentum-like intestinal anaerobe was specifically enhanced by the bacteroides present in mixed cultures and also by the addition to the growth medium of cell extracts from the bacteroides. The 7 alpha-dehydroxylating organism also possessed 7 alpha-hydroxysteroid dehydrogenase activity, and, in collaboration with a 7 beta-dehydrogenating organism, converted ursodeoxycholic acid (UDCA) into CDCA. Large quantities of lithocholic acids were produced from UDCA as well as CDCA in in vitro cocultures of these three kinds of microorganisms.

Anaerobiosis↗

PubMed1994

[Intrahepatic cholestasis in pregnancy. Its etiopathogenesis, prognosis and therapy].

Intrahepatic cholestasis of pregnancy (ICP) is a rare disease of unknown cause, recurrent, characterized by pruritus and, in some cases, mild jaundice. This cholestasis usually appears during the second half of pregnancy, and resolves in the early puerperium. ICP results in the elevation of serum total bile acids concentrations, mainly cholic acid, and abnormal routine liver function tests. Although maternal outcome is invariably good, an increased fetal risk has been reported, namely premature deliveries, fetal distress, and perinatal mortality. To avoid these deleterious consequences, strict fetal monitoring must be carried out during the final weeks of pregnancy, and the decision for delivery taken as soon as term or fetal maturity are achieved. The ursodeoxycholic acid (UDCA), that has been beneficial in other cholestatic liver diseases therapeutics, may become a promising drug in the treatment of ICP; nevertheless, due to the scarce experience with its use during ICP, and because its metabolism and mechanism of action is still poorly understood, it seems reasonable to test the effect of UDCA in these patients.

Cholestasis, Intrahepatic↗

PubMed1998

Decreased fecal bile acid output in patients with coronary atherosclerosis.

In most patients with atherosclerosis, the underlying metabolic derangement remains undefined. Animal experiments have suggested that the ability to produce and excrete large amounts of bile acids may be an adaptation mechanism to cholesterol overload protecting against the atherogenic effects of cholesterol. However, there are very few data on bile acid excretion in human atherosclerosis. In the present study, we have investigated fecal bile acid secretion in subjects with and without coronary artery disease. The target group consisted of 30 patients with proven coronary artery disease and the control group consisted of 27 matched subjects without clinical or laboratory evidence of coronary atherosclerosis. Fecal bile acids were measured by gas-liquid chromatography from 24-hr stool collections under a controlled diet. The patients excreted significantly less bile acids than the controls (325+/-135 vs. 592+/-223 mg/day, respectively, p < 0.0001). The difference was primarily due to a reduced excretion of secondary bile acids. Less than 50% of deoxycholate was excreted by patients (180+/-81 mg/day) as compared to controls (367+/-168 mg/day, p < 0.0002), while lithocholic acid excretion was 111+/-62 mg/day in patients vs. 190 +/-70 mg/day in controls (p < 0.005). The fecal output of the two primary bile acids, cholic and chenodeoxycholic acid, did not differ significantly between patients and controls. The fecal output of total bile acids correlated with that of both secondary bile acids in patients as well as in controls. These findings suggest that patients with coronary heart disease are unable to excrete adequate amounts of bile acids to rid themselves of excess cholesterol, even if they are able to maintain a plasma cholesterol level comparable to that of healthy controls.

Aged↗

PubMed1986

Selective inhibition of long-chain fatty acid uptake in short-term cultured rat hepatocytes by an antibody to the rat liver plasma membrane fatty acid-binding protein.

Uptake of long-chain fatty acids by short-term cultured hepatocytes was studied. Rat hepatocytes, which were cultured for 16 h on plastic dishes (3.6 X 10(6) cells/dish), were incubated with [3H]oleate in the presence of various concentrations of bovine serum albumin as a function of the concentration of unbound [3H]oleate in the medium. At 37 degrees C initial uptake velocity (V0) was saturable (Km = 9 X 10(-8) M; Vmax = 835 pmol/min per mg protein). V0 was temperature dependent with an optimum at 37 degrees C and markedly reduced at 4 degrees C and 70 degrees C. To evaluate the biologic significance of a previously isolated rat liver plasma membrane fatty acid-binding protein as putative carrier protein in the hepatocellular uptake of fatty acids, cultured hepatocytes were treated with a monospecific rabbit antibody (IgG-fraction) to this membrane protein or the IgG-fraction of the pre-immune serum as controls. Uptake kinetics of [3H]oleate in antibody pretreated short-term cultured hepatocytes revealed a depression of Vmax by 70%, while Km was only reduced by 16% compared to controls, indicating a predominant non-competitive type of inhibition. V0 of a variety of long-chain fatty acids (oleic acid, arachidonic acid, palmitic acid, stearic acid) was reduced by 56-69%, while V0 of [35S]sulfobromophthalein, [3H]cholic acid and [14C]taurocholic acid remained unaltered. These data support the concept that in the system of cultured hepatocytes, uptake of long-chain fatty acids is mediated by the rat liver plasma membrane fatty acid-binding protein.

Animals↗

PubMed1997

Effects of ursodeoxycholic acid on conjugated bile acids and progesterone metabolites in serum and urine of patients with intrahepatic cholestasis of pregnancy.

BACKGROUND/AIMS AND METHODS: The mechanism(s) behind the effects of ursodeoxycholic acid on serum steroid sulphate profiles in patients with intrahepatic cholestasis of pregnancy is not clear. Conjugated progesterone metabolites and bile acids have therefore been analysed in serum and urine of patients with intrahepatic cholestasis of pregnancy before and during treatment with ursodeoxycholic acid using chromatographic and mass spectrometric methods. RESULTS: The concentration of glycine-/taurine-conjugated bile acids decreased from 8.9+/-3 micromol/l (mean+/-SEM) before treatment to 1.8+/-0.6 micromol/l during treatment with ursodeoxycholic acid. The total bile acid excretion in urine decreased from 56+/-14 to 32+/-5.6 micromol/g creatinine. The proportion of cholic acid in serum and urine, and of 1beta-, 2beta- and 6alpha-hydroxylated cholic acids in urine decreased markedly during ursodeoxycholic acid while the percentages of 3alpha,12alpha-dihydroxy-3-oxo-4-cholenoic acid and chenodeoxycholic acid were unchanged. The levels in serum and excretion in urine of sulphated steroids decreased during ursodeoxycholic acid, by 45-49% for disulphates and 33-35% for monosulphates. The ratios of 3alpha- to 3beta-hydroxysteroid disulphates were lowered by ursodeoxycholic acid from 1.1 (mean) to 0.68 in serum, and from 1.2 to 0.70 in urine. The corresponding ratios for monosulphates before and during ursodeoxycholic acid were 6.9 and 4.5, respectively, in serum, and 21 and 5.2, respectively, in urine. The major monosulphates in urine, dominated by 5alpha-pregnane-3alpha, 20alpha-diol, were also conjugated with N-acetylglucosamine. The excretion of these double conjugates decreased from 27+/-8.4 to 15+/-5.3 micromol/g creatinine during ursodeoxycholic acid. In contrast to sulphated steroids, the concentrations of glucuronides were unchanged in serum and their excretion in urine tended to increase during ursodeoxycholic acid. The metabolism of ursodeoxycholic acid was similar to that described in nonpregnant subjects. In addition to metabolites hydroxylated in the 1beta-, 5beta-, 6alpha/beta and 22-positions, a 4-hydroxy-ursodeoxycholic acid was tentatively identified. This occurred predominantly as a double conjugate with glycine/taurine and glucuronic acid, as did other 4-hydroxylated bile acids of probable foetal origin. CONCLUSIONS: The results are compatible with the contention that ursodeoxycholic acid stimulates the biliary excretion of sulphated progesterone metabolites, particularly those with a 3alpha-hydroxy-5alpha(H) configuration and disulphates. The effect(s) appears to be independent of the stimulation of bile acid secretion. An effect of ursodeoxycholic acid on the reductive metabolism of progesterone cannot be excluded.

Bile Acids and Salts↗

PubMed1982

Bile acid transformation by the intestinal flora and cholesterol saturation in bile. Effects of Streptococcus faecium administration.

In 8 normal subjects the daily administration for 30 days of at least 750 X 10(6) Streptococcus faecium, a bacteria producing substances acting against Clostridia and other intestinal microorganisms reduced the cholesterol saturation and the molar percentage of deoxycholic acid (DCA) in bile. The percentage of cholic acid (CA) and chenodeoxycholic acid (DCA) increased significantly in feces, whereas lithocholic acid (LCA) decreased from 49.2 to 40.5%. In vitro fecal samples of subjects taking S. faecium transformed more slowly CA to DCA and CDCA to LCA. Moreover, 7-ketolithocholic seems an intermediate step in the biotransformation of CDCA to LCA. During SF administration, the anaerobic bacteria count of feces decreases, whereas aerobic bacteria increase; the changes of fecal flora may reduce the degradation of primary bile acids influencing the bile acid composition in both the bile and the intestine.

Adult↗

PubMed1993

[Antioxidant effect of vitamin E in experimental hyperlipidemia].

The effect of Vitamin E treatment was studied in experimental hyperlipidaemia. The male Wistar rats got control diet and parallel fat rich diet contained 2% cholesterol, 0.5% cholic acid and 20% sunflower oil added into LATI food during 9 days. The treated hyperlipidemic animals got vitamin E for 9 days in daily 8.56 mg/b.w.kg dose mixed in food. The effect of antioxidant treatment on changes of lipid peroxidation, content of diene conjugates, thiobarbituric acid reactive products and natural scavenger capacity of rat liver homogenates and microsome fractions were measured by spectrophotometric and luminometric methods. Fatty acid composition of lipid fraction of samples was determined by capillary gas chromatography. Vitamin E in hyperlipidemia increased the natural scavenger capacity of liver and decreased the level of thiobarbituric acid reactive products and dien conjugates. There was no change in fatty acid composition of samples on effect of vitamin E antioxidant treatment.

Animals↗

PubMed1982

Comparative effects of soy and casein protein on plasma cholesterol concentrations.

The effects of soy and casein protein on cholesterol metabolism were determined under normocholesterolemic and hypercholesterolemic conditions in male Wistar rats and in Swiss White mice. Hypercholesterolemia was induced by feeding cholesterol and cholic acid in the diet for a period of 2 weeks. Our results demonstrate that there are significant species differences. The hypercholesterolemic effect of exogenous cholesterol was more pronounced in the mouse than in the rat. The rats fed the basal (no cholesterol, no cholic acid) semisynthetic diet containing either soy or casein had plasma cholesterol concentrations similar to those observed in chow-fed controls. However, plasma cholesterol concentrations in the mice fed the basal semisynthetic diet containing either of the two proteins were significantly elevated compared to the control mice fed commercial chow. Rat data demonstrate that the hypercholesterolemia induced by exogenous cholesterol administration is of a lesser magnitude in the presence of soy compared to casein as a dietary protein source. The mice data show that the concentrations of hepatic and biliary cholesterol and plasma triglycerides and in response to exogenous cholesterol are significantly lower in the soy protein diet compared to the casein protein diet.

Animals↗

PubMed1982

Postprandial serum bile acids in resected and non-resected patients with Crohn's disease.

Fasting and postprandial serum conjugates of cholic acid (CCA) and chenodeoxycholic acid (CCDA) were determined by radioimmunoassay in 46 healthy individuals and 15 patients with Crohn's disease (CD), 7 bowel-resected and 8 non-resected. All patients had normal conventional liver test results, and fasting values of CCA and CCDA were within the reference ranges. Two findings appeared: the mean postprandial increases in CCA and CCDA were both lower in CD patients than than in healthy individuals, and the postprandial increase in CCA was lower in the resected patients than in the non-resected, whereas the postprandial increase in CCDA was the same in the resected and the non-resected patients. These findings show that in CD patients, whether resected or not, the postprandial levels of bile acids are low. This could reflect a decreased absorptive capacity of bile acids in the small intestine. The finding that postprandial CCA, but not CCDA, was lower in resected than in non-resected patients may reflect different sites of CCA and CCDA absorption.

Adult↗