Effects of treatment with deoxycholic acid and chenodeoxycholic acid on the hepatic synthesis of cholesterol and bile acids in healthy subjects

Hepatology ◽  
2001 ◽  
Vol 33 (5) ◽  
pp. 1189-1193 ◽  
Author(s):  
C Einarsson
Keyword(s):  
Bile Acids ◽  
Chenodeoxycholic Acid ◽  
Healthy Subjects ◽  
Deoxycholic Acid ◽  
Hepatic Synthesis

Radioimmunoassay of conjugated cholic acid, chenodeoxycholic acid, and deoxycholic acid from human serum, with use of 125I-labeled ligands.

1979 ◽  
Vol 25 (2) ◽  
pp. 264-268 ◽  
Author(s):  
O Mäentausta ◽  
O Jänne
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Cholic Acid ◽  
Chenodeoxycholic Acid ◽  
Deoxycholic Acid ◽  
Serum Samples ◽  
Analytical Recovery ◽  
Hepatobiliary Diseases ◽  
Polyethylene Glycol Precipitation ◽  
Free Serum

Abstract We describe a method for radioimmunoassay of conjugated cholic acid, chenodeoxycholic acid, and deoxycholic acid in serum. In the method, 125I-labeled bile acid conjugates are used as the tracers along with antibodies raised against individual bile acid-bovine serum albumin conjugates. Antibody-bound and free bile acids were separated by polyethylene glycol precipitation (final concentration, 125 g/L). Before radioimmunoassay, 0.1-mL serum samples were precipitated with nine volumes of ethanol, and portions from the supernate were used in the assays. The lowest measurable amounts of the bile acids, expressed as pmol/tube, were: cholic acid conjugates, 2; chenodeoxycholic acid conjugates, 0.5; and deoxycholic acid conjugates. 2. Analytical recovery of bile acids added to bile acid-free serum ranged from 85 to 110%; intra-assay and inter-assay CVs ranged from 3.2 to 5.3% and from 5.3 to 12.2%, respectively. Concentrations (mean +/- SD) of the bile acid conjugates in serum from apparently healthy women and men (in mumol/L) were: cholic acid conjugates, 0.43 +/- 0.17 (n = 126); chenodeoxycholic acid conjugates, 0.47 +/- 0.23 (n = 111); and deoxycholic acid conjugates, 0.33 +/- 0.11 (n = 96). The values for primary bile acids were greatly increased in patients with various hepatobiliary diseases.

scholarly journals Preparation of the 3-monosulphates of cholic acid, chenodeoxycholic acid and deoxycholic acid

1976 ◽  
Vol 155 (2) ◽  
pp. 401-404 ◽  
Author(s):  
E S. Haslewood ◽  
G A. D. Haslewood
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
Bile Acids ◽  
Cholic Acid ◽  
Chenodeoxycholic Acid ◽  
Deoxycholic Acid ◽  
Single Step ◽  
Acid Sulphate

1. The 3-sulphates of cholic, chenodeoxycholic and deoxycholic acids were prepared as crystalline disodium salts. 2. The method described shows that it is possible to prepare specific sulphate esters of polyhydroxy bile acids and to remove protecting acyl groups without removing the sulphate. 3. A study of bile acid sulphate solvolysis showed that none of the usual methods give the original bile acid in major yield in a single step. 4. An understanding of the preparation, properties and methods of solvolysis of bile acid sulphates is basic for investigations of cholestasis and liver disease.

Influence of Deoxycholic Acid Feeding on the Elimination of Cholesterol in Normolipaemic Subjects

1974 ◽  
Vol 47 (5) ◽  
pp. 425-433
Author(s):  
K. Einarsson ◽  
K. Hellström ◽  
M. Kallner
Keyword(s):  
Bile Acid ◽  
Total Synthesis ◽  
Bile Acids ◽  
Cholic Acid ◽  
Chenodeoxycholic Acid ◽  
Deoxycholic Acid ◽  
Cholesterol Metabolism ◽  
Pool Size ◽  
Faecal Excretion ◽  
The Mean

1. The turnover of [24−14C]cholic acid and [3H]chenodeoxycholic acid and the faecal excretion of neutral steroids were studied in six normolipaemic subjects before and during the ingestion of 1.3–2.6 mmol (0.5–1.0 g) of deoxycholic acid/day. Before the second study the subjects had been fed deoxycholic acid for 2 weeks. 2. The administration of deoxycholic acid did not appear to influence cholesterol metabolism as judged by the absence of change in the serum concentrations and the overall transformation into primary bile acids and neutral faecal steroids. 3. During the deoxycholic acid feeding period the mean total synthesis of bile acids was reduced by about 30%, corresponding to approximately 0.25 mmol (100 mg)/day. In one subject the pool size and in another the synthesis of cholic acid remained unchanged; otherwise the cholic acid pool size and its rate of formation decreased in all subjects. No consistent effects were observed with regard to the turnover of chenodeoxycholic acid. 4. Assuming that the bile acid turnover is equivalent to bile acid excretion then the total amount of cholesterol eliminated as bile acids and neutral faecal steroids averaged between 1.6 and 1.8 mmol/day before and during the administration of deoxycholic acid.

scholarly journals Effects of bile acids on human airway epithelial cells: implications for aerodigestive diseases

2017 ◽  
Vol 3 (1) ◽  
pp. 00107-2016 ◽  
Author(s):  
Adil Aldhahrani ◽  
Bernard Verdon ◽  
Chris Ward ◽  
Jeffery Pearson
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Lung Disease ◽  
Bile Acids ◽  
Chenodeoxycholic Acid ◽  
Deoxycholic Acid ◽  
Lithocholic Acid ◽  
Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial

Gastro-oesophageal reflux and aspiration have been associated with chronic and end-stage lung disease and with allograft injury following lung transplantation. This raises the possibility that bile acids may cause lung injury by damaging airway epithelium. The aim of this study was to investigate the effect of bile acid challenge using the immortalised human bronchial epithelial cell line (BEAS-2B).The immortalised human bronchial epithelial cell line (BEAS-2B) was cultured. A 48-h challenge evaluated the effect of individual primary and secondary bile acids. Post-challenge concentrations of interleukin (IL)-8, IL-6 and granulocyte−macrophage colony-stimulating factor were measured using commercial ELISA kits. The viability of the BEAS-2B cells was measured using CellTiter-Blue and MTT assays.Lithocholic acid, deoxycholic acid, chenodeoxycholic acid and cholic acid were successfully used to stimulate cultured BEAS-2B cells at different concentrations. A concentration of lithocholic acid above 10 μmol·L−1 causes cell death, whereas deoxycholic acid, chenodeoxycholic acid and cholic acid above 30 μmol·L−1 was required for cell death. Challenge with bile acids at physiological levels also led to a significant increase in the release of IL-8 and IL6 from BEAS-2B.Aspiration of bile acids could potentially cause cell damage, cell death and inflammation in vivo. This is relevant to an integrated gastrointestinal and lung physiological paradigm of chronic lung disease, where reflux and aspiration are described in both chronic lung diseases and allograft injury.

Oxidation of primary bile acids by a 7α-hydroxysteroid dehydrogenase elaborating Clostridium bifermentans soil isolate

1987 ◽  
Vol 33 (8) ◽  
pp. 663-669 ◽  
Author(s):  
J. Derek Sutherland ◽  
C. Noel Williams ◽  
Donna M. Hutchison ◽  
Lillian V. Holdeman
Keyword(s):  
Bile Acids ◽  
Chenodeoxycholic Acid ◽  
Deoxycholic Acid ◽  
Specific Activity ◽  
Hydroxysteroid Dehydrogenase ◽  
Ph Optimum ◽  
Reactive Blue 2 ◽  
Cell Extracts ◽  
Initial Drop ◽  
Clostridium Bifermentans

A gram-positive, rod-shaped anaerobe (strain F-6) was isolated from soil. This organism was identified by cellular morphology as well as fermentative and biochemical data as Clostridium bifermentans. Strain F-6 formed 7-ketolithocholic acid from chenodeoxycholic acid and 7-ketodeoxycholic acid from cholic acid in whole cell cultures, but did not transform deoxycholic acid, ursodeoxycholic acid, or ursocholic acid. This reaction is reversible. The structures of 7-ketolithocholic acid and 7-ketodeoxycholic acid were verified by mass spectroscopy and by thin-layer chromatography using Komarowsky's spray reagent. When incubated with the strain F-6 glycine and taurine conjugates of the primary bile acids were partially hydrolyzed and transformed to 7-keto products. Optimal yields of 7-ketolithocholic acid and 7-ketodeoxycholic acid were obtained after 78 h of incubation. Culture pH changed with time and was characterized by an initial drop (1.1 pH units) and a gradual increase back to the starting pH (7.3). Corroborating these observations, an inducible, NADP-dependent, 7α-hydroxysteroid dehydrogenase was demonstrated in cell extracts of strain F-6. A trace of NAD-dependent 7α-hydroxysteroid dehydrogenase was also found. A substantial increase in the specific activity of the NADP-dependent 7α-hydroxysteroid dehydrogenase was observed when either 7-ketolithocholic acid, chenodeoxycholic acid, or deoxycholic acid was included in the growth medium. Optimal induction of the NADP-dependent 7α-hydroxysteroid dehydrogenase was achieved with 0.3–0.4 mM 7-ketolithocholic acid. Production of the enzyme(s) was optimal at 6–8 h of growth and the 7α-hydroxysteroid dehydrogenases had a pH optimum of approximately 11. The 7α-hydroxysteroid dehydrogenase from strain F-6 was purified 12-fold by triazine dye affinity chromatography with reactive blue 2 (Cibacron blue) agarose (95% yield). It was successfully lyophilized into a stable powder form.

scholarly journals Bile acids inhibit human purinergic receptor P2X4 in a heterologous expression system

2019 ◽  
Vol 151 (6) ◽  
pp. 820-833 ◽  
Author(s):  
Alexandr V. Ilyaskin ◽  
Florian Sure ◽  
Viatcheslav Nesterov ◽  
Silke Haerteis ◽  
Christoph Korbmacher
Keyword(s):  
Ion Channel ◽  
Bile Acids ◽  
Cholic Acid ◽  
Chenodeoxycholic Acid ◽  
Deoxycholic Acid ◽  
Purinergic Receptor ◽  
Expression System ◽  
Inhibitory Effect ◽  
Xenopus Laevis Oocytes ◽  
Dependent Manner

We recently demonstrated that bile acids, especially tauro-deoxycholic acid (t-DCA), modify the function of the acid-sensing ion channel ASIC1a and other members of the epithelial sodium channel (ENaC)/degenerin (DEG) ion channel family. Surprisingly, ASIC1 shares a high degree of structural similarity with the purinergic receptor P2X4, a nonselective cation channel transiently activated by ATP. P2X4 is abundantly expressed in the apical membrane of bile duct epithelial cells and is therefore exposed to bile acids under physiological conditions. Here, we hypothesize that P2X4 may also be modulated by bile acids and investigate whether t-DCA and other common bile acids affect human P2X4 heterologously expressed in Xenopus laevis oocytes. We find that application of either t-DCA or unconjugated deoxycholic acid (DCA; 250 µM) causes a strong reduction (∼70%) of ATP-activated P2X4-mediated whole-cell currents. The inhibitory effect of 250 µM tauro-chenodeoxycholic acid is less pronounced (∼30%), and 250 µM chenodeoxycholic acid, cholic acid, or tauro-cholic acid did not significantly alter P2X4-mediated currents. t-DCA inhibits P2X4 in a concentration-dependent manner by reducing the efficacy of ATP without significantly changing its affinity. Single-channel patch-clamp recordings provide evidence that t-DCA inhibits P2X4 by stabilizing the channel’s closed state. Using site-directed mutagenesis, we identifiy several amino acid residues within the transmembrane domains of P2X4 that are critically involved in mediating the inhibitory effect of t-DCA on P2X4. Importantly, a W46A mutation converts the inhibitory effect of t-DCA into a stimulatory effect. We conclude that t-DCA directly interacts with P2X4 and decreases ATP-activated P2X4 currents by stabilizing the closed conformation of the channel.

scholarly journals Pseudomonas μtant strains that accumulate androstane and seco-androstane intermediates from bile acids

1987 ◽  
Vol 243 (1) ◽  
pp. 15-21 ◽  
Author(s):  
R A Leppik ◽  
D J Sinden
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Chenodeoxycholic Acid ◽  
Deoxycholic Acid ◽  
Major Product ◽  
Pseudomonas Spp ◽  
Mutant Strains ◽  
The One ◽  
The Relationship

Transposon mutant strains which were affected in bile acid catabolism were isolated from four Pseudomonas spp. Two of the mutant groups isolated were found to accumulate 12 alpha-hydroxyandrosta-1,4-diene-3,17-dione as the major product from deoxycholic acid. Strains in one of these two groups were able to grow on steroids such as chenodeoxycholic acid, which lacks a 12 alpha-hydroxy function, whereas the one member of the second group could not. With chenodeoxycholic acid, this latter strain accumulated a yellow muconic-like derivative, tentatively identified as 3,7-dihydroxy-5,9,17-trioxo-4(5),9(10)-disecoandrosta-1(10)2 -dien-4-oic acid. Members of two further mutant groups accumulated either 12 beta-hydroxyandrosta-1,4-diene-3,17-dione or 3,12 beta-dihydroxy-9(10)-secoandrosta-1,3,5(10)-triene-9,17-dione as the major product from deoxycholic acid. The relationship between the catabolism of m- and p-cresol, 3-ethylphenol and the bile acids was also examined.

Results with six "kit" radioimmunoassays for primary bile acids in human serum intercompared.

1980 ◽  
Vol 26 (12) ◽  
pp. 1677-1682 ◽  
Author(s):  
A Roda ◽  
E Roda ◽  
R Aldini ◽  
M Capelli ◽  
D Festi ◽  
...  
Keyword(s):  
Human Serum ◽  
Bile Acids ◽  
Cholic Acid ◽  
Chenodeoxycholic Acid ◽  
Healthy Subjects ◽  
Liquid Scintillation ◽  
Normal Values ◽  
Affinity Constant ◽  
Analytical Recovery ◽  
High Concentrations

Abstract We examined six radioimmunoassay procedures for measuring primary bile acids in human serum (two 3H-labeled and four 125I-labeled). A significant (p < 0.01) correlation was observed between measurements in the assay both for cholic acid and chenodeoxycholic acid, at low and high concentrations of serum bile acids. All kits were acceptable with respect to accuracy, precision, stability, and analytical recovery. All six procedures gave similar results for chenodeoxycholic and cholic acid in sera of 80 healthy subjects; the agreement was also close when the two primary bile acids were compared with their sum in serum. Normal values ranged from 0.4 to 2.5 mumol/L for conjugated chenodeoxycholic acid and from 0.3 to 1.5 mumol/L for conjugated cholic acid. The 125I assays do not require liquid-scintillation equipment but 125I induces a decrease in the affinity constant of antibody. The sensitivity of the assays was still adequate for measuring bile acids in the serum of healthy fasting persons and liver-disease patients.

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