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PubMed1995

Changes in the level of 7 alpha-hydroxy-3-oxo-4-cholestenoic acid in cerebrospinal fluid after subarachnoid hemorrhage.

A high concentration of a type of cholic acid, 7 alpha-hydroxy-3-oxo-4-cholestenoic acid, is observed in the content of chronic subdural hematoma. To investigate the possible causes, the level of this compound was measured in the cerebrospinal fluid of patients who underwent surgery for aneurysmal subarachnoid hemorrhage or non-hemorrhagic diseases. The maximum level was significantly higher in the aneurysmal subarachnoid hemorrhage patients, indicating that surgical intervention did not cause the postoperative increase in the level of this compound in the cerebrospinal fluid. Monitoring of plasma levels showed no postoperative increase. In vitro culture of a mixture of arterial blood and cerebrospinal fluid failed to show the de novo production of this compound. These results strongly suggest extrahepatic intracranial production of this cholic acid occurs in subarachnoid hemorrhage. The high concentration of this compound in both chronic subdural hematoma and subarachnoid hemorrhage suggests a possible role for 7 alpha-hydroxy-3-oxo-4-cholestenoic acid in intracranial hemorrhagic disorders.

Adult↗

PubMed2001

Transcriptional regulation of the human sterol 27-hydroxylase gene (CYP27) and promoter mapping.

Recent evidence suggests that sterol 27-hydroxylase may play a role in cholesterol homeostasis and affect atherogenesis. The major objective of the study was to map and characterize the sterol 27-hydroxylase (CYP27) promoter region. Here we show that CYP27 gene has a TATA-less promoter and transcription initiates at a cluster of sites. The basic promoter is located between -166 and -187 bp from the translation initiation site. Possible positive transcription regulation sites are located at position -187 to -320 and -857 to -1087 bp. A negative transcription regulator site is located in position -320 to -413 bp. An enhancer sequence is located upstream to position -1087. CYP27 is upregulated by dexamethasone and downregulated by cyclosporin A and cholic acid. The dexamethasone responsive element is located between 1087 and 678 bp upstream to the putative ATG. Cyclosporin A affects bile acid metabolism by repressing CYP27 at the transcriptional level. The cyclosporin A- responsive element is mapped to between 1087 and 4000 bp upstream of the ATG. Cholic acid represses sterol 27-hydroxylase mRNA level by affecting the stability of its mRNA. The results obtained here imply that CYP27 has a potentially important role in cholesterol homeostasis in human cells, and is regulated by several substances that were previously shown to affect bile acid metabolism.

Base Sequence↗

PubMed2000

A buckwheat protein product suppresses gallstone formation and plasma cholesterol more strongly than soy protein isolate in hamsters.

This study was conducted to investigate the effects of a buckwheat protein product (BWP) on plasma cholesterol, gallbladder bile composition and fecal steroid excretion in hamsters fed diets with 5 g/kg cholesterol. Diets also contained 200 g/kg of casein, soy protein isolate (SPI) or BWP as protein sources. After 2 wk, plasma and liver concentrations of cholesterol in the hamsters fed BWP were significantly lower than those in the hamsters fed casein and SPI. The molar proportion of cholesterol in gallbladder bile was significantly lower in the BWP group than in the other groups, whereas that of bile acids was slightly higher in the BWP group (P </= 0.05), resulting in the lowest lithogenic index in the BWP group. None of the hamsters fed BWP had gallstones, whereas they were present in some of the hamsters fed other proteins. Compared with casein intake, BWP intake resulted in significantly higher ratios of cholic acid to chenodeoxycholic acid and of cholic acid to lithocholic acid in the gallbladder bile. The excretions of fecal neutral and acidic steroids were markedly higher in the BWP group compared with the other groups (P </= 0.05). SPI intake also significantly lowered cholesterol level in gallbladder bile and caused higher fecal bile acids compared with casein intake, but the effects were significantly less than those of BWP (P </= 0.05). The results suggest that BWP suppresses gallstone formation and cholesterol level more strongly than SPI by enhancing bile acid synthesis and fecal excretion of both neutral and acidic steroids.

Animals↗

PubMed1975

Biliary bile acid composition in Wilson's disease.

Biliary bile acid composition and pattern of bile acid conjugation with glycine or taurine were found to be within normal limits in six patients with documented Wilson's disease. Four patients had previous biopsy evidence of cirrhosis (three with active hepatitis), but most conventional liver function tests gave normal results at the time of the study. Serum levels of conjugates of cholic acid, measured by radioimmunoassay, were not increased. However, plasma disappearance if intravenously injected glycine conjugate of cholic acid was significantly delayed in all subjects, suggesting that this is a more sensitive test of hepatic excretory function and may be of value for assessing hepatic function in patients with this rare genetic disorder. No evidence of a primary disturbance in bile acid metabolism was found in these patients.

Adolescent↗

PubMed1987

Occurrence of both (25R)- and (25S)-3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acids in urine from an infant with Zellweger's syndrome.

Urine from a patient with Zellweger's syndrome was examined for bile acids after fractionation into three groups according to mode of conjugation. 3 alpha,7 alpha,12 alpha-Trihydroxy-5 beta-cholestanoic acid was the predominant bile acid of the unconjugated and glycine-conjugated bile acid fractions. Smaller amounts of cholic acid and 1 beta-, 6 alpha-, 24-, and 26-hydroxylated derivatives of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid were found in both fractions in similar proportions. The bile acid spectrum of the taurine-conjugated bile acid fraction was different from those of the other two fractions in the occurrence of two new compounds as the major constituents. These compounds were tentatively identified as two epimers at C-23 of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestano-26,23-lactone, which were probably artifacts formed from the corresponding tetrahydroxycholestanoic acids during the procedures for extraction after hydrolysis. High-performance liquid chromatographic analysis revealed that 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid excreted into the urine as the unconjugated form consisted of a mixture of (25R)- and (25S)-isomers in the ratio of about 7:3.

Bile Acids and Salts↗

PubMedDate not supplied

[Disturbance of the intensity of secretion and chemical composition of bile in liver dystrophy induced by carbon tetrachloride].

Liver dystrophy induced by carbon tetrachloride results in inhibition of intensity of bile secretion and cholate formation and upsets discharge of bilirubin and cholesterol with bile. Inhibition of cholate synthesis might be accounted for by repressed production of deoxycholic and cholic acid from cholesterol as well as by repressed conjugation of cholic acid with taurine and glycine. Cessation of carbon tetrachloride injections is followed by steady restoration of bile formation: first of all is discharge of bilirubin restored, then discharge of cholesterol, and much later intensity of bile discharge and formation of bile acids.

Animals↗

PubMed1984

Abnormal bile acid pool and composition in neonates of spontaneously diabetic Wistar BB rats and its change during development.

Streptozotocin-induced diabetes during pregnancy in rats causes a decrease in primary bile acid pool in neonates. To rule out direct drug effect on the fetus as the basis for this change, studies of bile acid pool and composition at birth and during subsequent development was carried out in neonates of spontaneously diabetic Wistar BB rats and compared to control neonates. The cholic acid pool in neonates of diabetic rats was lower when compared to control neonates at birth. The pool of secondary bile acids was markedly increased in neonates of diabetic rats, with increases in lithocholic and 3 beta,12 alpha-dihydroxycholanoic acid. With age, the cholic acid pool of neonates from diabetic rats was increased and at 3 months of age it was actually higher than in control neonates. The pool of chenodeoxycholic at diabetes onset age was lower in neonates of diabetic rats. HDL-cholesterol was lower in neonates of diabetic rats at 1 week, but this reversed at 3 months of age. These studies firmly establish that neonates of diabetic rats have abnormal bile acid pool and composition at birth which changes to adult diabetic pattern with age.

Age Factors↗

PubMed2002

[Disturbances in biliary secretion during tissue hypoxia and attempts at their corrections].

In acute experiments on rats in vivo the stimulating effects of hydrophilic cholic acids (CA and UDCA) on the bilification and their inhibiting by rotenone have been shown. The secretion of CA and UDCA under rotenone have been determined to be activated. The mechanisms of the influence of the cholic acids on the secretory function of the hepatocytes have being discussed. It has been concluded that NADH-dehydrogenase link in the respiratory chain is not involved in the activating effects by CA and UDCA.

Animals↗

PubMed2004

Bile acids are new products of a marine bacterium, Myroides sp. strain SM1.

Strain SM1 was isolated as a biosurfactant-producing microorganism from seawater and presumptively identified as Myroides sp., based on morphology, biochemical characteristics and 16S rDNA sequence. The strain produced surface-active compounds in marine broth, which were purified, using emulsification activity for n-hexadecane as an indicator. The purified compounds were identified by thin-layer chromatography, (1)H- and (13)C-NMR spectra and fast atom bombardment mass spectrometry as cholic acid, deoxycholic acid and their glycine conjugates. Type strains of the genus Myroides, M. odoratus JCM7458 and M. odoramitimus JCM7460, also produced these compounds. Myroides sp. strain SM1 possessed a biosynthetic route to cholic acid from cholesterol. Thus, bile acids were found as new products of prokaryotic cells, genus Myroides.

Bile Acids and Salts↗

PubMed2000

Abnormal hepatic sinusoidal bile acid transport in an Amish kindred is not linked to FIC1 and is improved by ursodiol.

BACKGROUND & AIMS: The mechanism for abnormal hepatic bile acid transport was investigated in an 18-month-old Amish boy who presented with pruritus, poor growth, and severe bleeding episodes. Serum bilirubin, gamma-glutamyltranspeptidase, and cholesterol levels were normal, but prothrombin time and partial thromboplastin time were prolonged and bone alkaline phosphatase level was elevated. METHODS AND RESULTS: Cholic acid plus chenodeoxycholic acid levels measured by capillary gas-chromatography were 32 times higher than control in serum (34.7 vs. 1.1+/-0.4 microg/dL) but were not detected in liver and were reduced in gallbladder bile. Treatment with ursodiol, a more hydrophilic bile acid, improved pruritus, produced 37% weight gain, and after 2 years reduced serum primary bile acid concentrations about 85%, while accounting for 71% of serum and 24% of biliary bile acid conjugates. On ursodiol therapy, hepatic bile acid synthesis was enhanced 2-fold compared with controls, and microscopy revealed chronic hepatitis without cholestasis. Three younger sisters with elevated serum bile acids responded positively to ursodiol. Microsatellite markers for the FIC1 (gene for Byler's disease) region in these 4 children were inconsistent with linkage to FIC1. CONCLUSIONS: Conjugated cholic acid and chenodeoxycholic acid were synthesized in the liver and secreted into bile but could not reenter the liver from portal blood and accumulated in serum. In contrast, unconjugated ursodiol entered the liver and was conjugated and secreted into bile. Thus, the enterohepatic circulation of all conjugated bile acids was interrupted at the hepatic sinusoidal basolateral membrane. Unconjugated ursodiol bypassed the hepatic uptake block to enlarge the biliary and intestinal bile acid pools. A mutation in FIC1 recognized among the Amish and linkage of the disorder to FIC1 were excluded.

Adenosine Triphosphatases↗

PubMed2004

Differentially-protected steroidal triamines; scaffolds with potential for medicinal, supramolecular, and combinatorial chemistry.

Cholic acid 2a has been converted into two new orthogonally-protected triamino scaffolds, 13 and 14. The synthesis proceeds via the bis-Boc-NH-substituted azide 10, for which an improved preparation is described. After removal of the Boc groups, the two axial amines are differentiated through a novel monoprotection employing 1-(2-nitrobenzenesulfonyloxy)-benzotriazole 29. Regioselectivity of > or 50 : 1 is achieved, presumably reflecting an exceptional sensitivity to steric hindrance. Protection of the remaining amino group as Boc or Alloc gives the scaffolds in approximately 40% overall yield from cholic acid. Scaffold 13 has been sequentially deprotected and derivatised with N-carbamoyl amino acids, to give a model for tripodal peptide libraries.

Amino Acids↗

PubMed1977

Failure of complete bile diversion and oral bile acid therapy in the treatment of homozygous familial hypercholesterolemia.

Two patients with nomozygous familial hypercholesterolemia, refractory to medical therapy, underwent complete bile diversion by common-duct ligation and cholecystostomy, in an attempt to arrest the progression of their xanthomatosis and atherosclerosis by depletion of body cholesterol. Clofibrate was given after operation to one patient, and cholic acid to both, in an effort to enhance further the negative sterol balance. Bile diversion produced an increase of six to eight times in gastrointestinal sterol output, which was not increased further by either clofibrate or cholic acid therapy. Despite a calculated sterol loss of 560 g over 14 months in one patient and 400 g over 10 months in the other, neither plasma cholesterol nor xanthoma size decreased. Continuity of the biliary tree was therefore restored. The data suggest that patients with homozygous familial hypercholesterolemia respond to even massive gastrointestinal sterol depletion with equal increases in sterol synthesis.

Administration, Oral↗

PubMed1988

The synthesis of glycine conjugated 3-oxo-bile acids.

The glycine conjugates of the 3-oxo-derivatives of lithocholic, deoxycholic, chenodeoxycholic and cholic acids have been synthesized from their respective parent bile acid using established procedures. The reaction sequence involved oxidation using either chromic acid or silver carbonate--Celite followed by a conjugation step employing the peptide coupling reagent N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline. The final products were obtained in both high yield and purity for use as reference compounds in the analysis of conjugated bile acids in bile and faecal samples by high performance liquid chromatography. Analysis of the prepared 3-oxo-glycobile acids by fast atom bombardment negative ion mass spectrometry, infrared spectroscopy and nuclear magnetic resonance proton spectroscopy is also discussed along with the thin-layer chromatographic properties.

Chemical Phenomena↗

PubMed1977

Individual bile acids in portal venous and systemic blood serum of fasting man.

The serum concentrations of cholic acid (C), chenodeoxycholic acid (CD), and deoxycholic acid (D) were determined in peripheral venous and portal venous blood from 10 otherwise healthy patients undergoing elective cholecystectomy. A highly specific and accurate gas chromatographic-mass spectrometric technique was used. Peripheral venous serum contained 0.49 +/- 0.16 (mean +/- SEM) mumole per liter of C, 1.55 +/- 0.32 mumoles per liter of CD, and 1.44 +/- 0.57 mumoles per liter of D. Arterial serum, obtained from 5 of the subjects, did not show any differences in bile acid concentrations compared to venous serum. In contrast, the portal venous content of each bile acid was several-fold greater, 6.14 +/- 1.20 mumoles per liter of C, 8.40 +/- 1.84 mumoles per liter of CD, and 6.18 +/- 2.27 mumoles per liter of D. The hepatic uptake of C was estimated to be about 90%, whereas that of CD and D was lower, about 70%. This difference in hepatic uptake between the individual bile acids was reflected in the relative composition of the total bile acids, which was 30:39:31 (C:CD:D) in portal venous serum and 13:50:37 in peripheral serum. Compared to common duct bile obtained simultaneously, the portal vein contained a greater proportion of CD. The relevance of the data obtained to our present concept of the enterohepatic circulation of bile acids is discussed, and it is suggested that the higher fasting level of CD compared to C in peripheral serum results from the combination of a lower fractional hepatic extraction and a higher portal venous input to the systemic circulation.

Aged↗

PubMed1986

Pancreatic carboxypeptidase hydrolysis of bile acid-amino conjugates: selective resistance of glycine and taurine amidates.

To find a possible explanation for the selective hepatic conjugation of bile acids with glycine or taurine, the N-acyl amidates of cholic acid and a number of amino acids and amino acid analogues were synthesized, and their susceptibility to hydrolysis by pancreatic juice, gastric juice, serum, or small intestinal mucosal enzymes was measured. Deconjugation by pure carboxypeptidase A and B was also examined, and hydrolysis by these tissue fluids and enzymes was compared with that mediated by a bacterial cholylglycine hydrolase. Human pancreatic juice efficiently hydrolyzed cholyl conjugates of all neutral-L-amino acids (cholyl-L-alanine, cholyl-L-valine, cholyl-L-leucine, and cholyl-L-tyrosine), except cholylglycine. The net hourly rate of hydrolysis (in micromoles per milligram protein per hour) increased when the terminal residue was aromatic or branched aliphatic, and appeared to be specific for L-alpha-amino acids as cholyl-beta-alanine and cholyl-D-valine were not cleaved. From cholyl glycylglycine, only the terminal glycine was efficiently removed. Cholyltaurine and cholyl conjugates with the methyl and propyl analogues of taurine were resistant to hydrolysis. Two basic amino acid conjugates (cholyl-L-lysine and cholyl-L-arginine) were cleaved, whereas conjugates of acidic amino acids (cholyl-aspartate and cholyl-cysteate) were not cleaved. Studies using pure enzymes showed that bovine carboxypeptidase A hydrolyzed the cholyl conjugates of the neutral L-alpha-amino acids with similar specificity as observed for the human pancreatic juice, whereas bovine carboxypeptidase B cleaved the basic amino acid conjugates. Cholyl-L-lysine and cholyl-L-arginine were also cleaved by serum and plasma, which are known to possess carboxypeptidase activity. Cholyl conjugates were not cleaved by gastric juice, by trypsin, or by homogenates of rat small intestinal mucosa. In contrast, all cholyl conjugates were cleaved by a bacterial cholylglycine hydrolase. These experiments indicate that glycine and taurine amidates of cholic acid differ from a number of other conjugates with neutral and basic amino acid in being resistant to hydrolysis by pancreatic and plasma carboxypeptidases.(ABSTRACT TRUNCATED AT 400 WORDS)

Amidohydrolases↗

PubMed1987

Intestinal involvement in progressive systemic sclerosis detected by increased unconjugated serum bile acids.

In patients with progressive systemic sclerosis, impaired motor function of the small intestine may lead to bacterial overgrowth causing diarrhoea, steatorrhoea and malabsorption. As unconjugated serum bile acids have been proposed as markers for small bowel bacterial overgrowth, we studied individual unconjugated serum bile acids in 36 patients with progressive systemic sclerosis. These patients had significantly higher serum concentrations of unconjugated cholic acid (median 0.18; range 0.05-30.75 v 0.09; 0.01-0.19 mumol/l, p less than 0.001) and chenodeoxycholic acid (0.10; 0.01-6.83 v 0.04; 0.01-0.39 mumol/l, p less than 0.025) than healthy controls (n = 16). This difference was mainly due to patients with diarrhoea (n = 10), who had significantly higher concentrations of unconjugated serum bile acids than patients with normal bowel habit (cholic acid median 0.55 v 0.16 mumol/l, p less than 0.001; chenodeoxycholic acid 0.75 v 0.07 mumol/l; p less than 0.005). All patients with raised unconjugated serum bile acids had oesophageal motility disorders. These results confirm a relationship between motility disorders and bacterial overgrowth in patients with progressive systemic sclerosis.

Bile Acids and Salts↗

PubMed2001

Controlled expansion of a molecular cavity in a steroid host compound.

Expansion of a molecular cavity is described by using elongation of the side chain of a bile acid host compound. Bishomocholic acid (2), which has a side chain that is longer by two methylene unit than cholic acid (1), includes many organic substances at 1:1 host:guest ratios. X-ray crystallographic studies revealed that 2 has two types of open host frameworks: a bilayer type and a crossing type. Both of them are isostructural to those of 1, indicating that they are robust against the elongation of the side chain. In the former type, the increment of the width of the host channel corresponds to that of the length of the molecular structures. Larger aromatic guest components such as 1-methylnaphthalene and 1-tetralone, are included in 2, but not in 1.

Bile Acids and Salts↗

PubMed1986

Bile acids and plasma high density lipoproteins: biliary lipid metabolism in fish eye disease.

Cholesterol in plasma high density lipoproteins (HDL) has been proposed to serve as preferential precursor for bile acid biosynthesis in the liver. Furthermore, a negative relationship between plasma levels of HDL cholesterol and biliary saturation with cholesterol has been reported in healthy females. We have performed metabolic studies on a female patient with fish eye disease, a familial condition where plasma HDL levels are reduced by 90% and the concentration of plasma triglycerides is moderately increased. Both the total production of bile acids and the net steroid 'balance' (reflecting total body cholesterol synthesis) were within the range seen in normolipidaemic as well as in hypertriglyceridaemic females. Also the biliary lipid composition and cholesterol saturation of bile were normal. A qualitative abnormality in the bile acid pattern was observed, however, in that the ratio between the synthesis of cholic acid and chenodeoxycholic acid was reduced. It is concluded that a low HDL cholesterol level is not necessarily associated with quantitative abnormalities of biliary lipid metabolism. The abnormal bile acid synthesis ratio may reflect changes in the hepatic precursor pools of cholesterol as the consequence of HDL deficiency, however.

Aged↗