Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones.Cholic Acids: The 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholanic acid family of bile acids in man, usually conjugated with glycine or taurine. They act as detergents to solubilize fats for intestinal absorption, are reabsorbed by the small intestine, and are used as cholagogues and choleretics.Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones.Lithocholic Acid: A bile acid formed from chenodeoxycholate by bacterial action, usually conjugated with glycine or taurine. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as cholagogue and choleretic.Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.Deoxycholic Acid: A bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent.Cholic Acid: A major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion.Bile: An emulsifying agent produced in the LIVER and secreted into the DUODENUM. Its composition includes BILE ACIDS AND SALTS; CHOLESTEROL; and ELECTROLYTES. It aids DIGESTION of fats in the duodenum.Cholelithiasis: Presence or formation of GALLSTONES in the BILIARY TRACT, usually in the gallbladder (CHOLECYSTOLITHIASIS) or the common bile duct (CHOLEDOCHOLITHIASIS).Xanthomatosis, Cerebrotendinous: An autosomal recessive lipid storage disorder due to mutation of the gene CYP27A1 encoding a CHOLESTANETRIOL 26-MONOOXYGENASE. It is characterized by large deposits of CHOLESTEROL and CHOLESTANOL in various tissues resulting in xanthomatous swelling of tendons, early CATARACT, and progressive neurological symptoms.Cholestanols: Cholestanes substituted in any position with one or more hydroxy groups. They are found in feces and bile. In contrast to bile acids and salts, they are not reabsorbed.Glycocholic Acid: The glycine conjugate of CHOLIC ACID. It acts as a detergent to solubilize fats for absorption and is itself absorbed.Xanthomatosis: A condition marked by the development of widespread xanthomas, yellow tumor-like structures filled with lipid deposits. Xanthomas can be found in a variety of tissues including the SKIN; TENDONS; joints of KNEES and ELBOWS. Xanthomatosis is associated with disturbance of LIPID METABOLISM and formation of FOAM CELLS.Cholagogues and Choleretics: Gastrointestinal agents that stimulate the flow of bile into the duodenum (cholagogues) or stimulate the production of bile by the liver (choleretic).Cholestenones: CHOLESTENES with one or more double bonds and substituted by any number of keto groups.Cholestanes: Derivatives of the saturated steroid cholestane with methyl groups at C-18 and C-19 and an iso-octyl side chain at C-17.Steroid 12-alpha-Hydroxylase: A liver microsomal cytochrome P450 enzyme that catalyzes the 12-alpha-hydroxylation of a broad spectrum of sterols in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP8B1gene, converts 7-alpha-hydroxy-4-cholesten-3-one to 7-alpha-12-alpha-dihydroxy-4-cholesten-3-one and is required in the synthesis of BILE ACIDS from cholesterol.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Cholenes: Unsaturated derivatives of cholane with methyl groups at C-10 and C-13 and a branched five-carbon chain at C-17. They must have at least one double bond in the ring system.Hydroxysteroid Dehydrogenases: Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.Glycochenodeoxycholic Acid: A bile salt formed in the liver from chenodeoxycholate and glycine, usually as the sodium salt. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is a cholagogue and choleretic.Steroid Hydroxylases: Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.Enterohepatic Circulation: Recycling through liver by excretion in bile, reabsorption from intestines (INTESTINAL REABSORPTION) into portal circulation, passage back into liver, and re-excretion in bile.Cholestanol: A cholesterol derivative found in human feces, gallstones, eggs, and other biological matter.Cholesterol 7-alpha-Hydroxylase: A membrane-bound cytochrome P450 enzyme that catalyzes the 7-alpha-hydroxylation of CHOLESTEROL in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP7, converts cholesterol to 7-alpha-hydroxycholesterol which is the first and rate-limiting step in the synthesis of BILE ACIDS.Taurochenodeoxycholic Acid: A bile salt formed in the liver by conjugation of chenodeoxycholate with taurine, usually as the sodium salt. It acts as detergent to solubilize fats in the small intestine and is itself absorbed. It is used as a cholagogue and choleretic.Gallbladder: A storage reservoir for BILE secretion. Gallbladder allows the delivery of bile acids at a high concentration and in a controlled manner, via the CYSTIC DUCT to the DUODENUM, for degradation of dietary lipid.Taurocholic Acid: The product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic.Gas Chromatography-Mass Spectrometry: A microanalytical technique combining mass spectrometry and gas chromatography for the qualitative as well as quantitative determinations of compounds.CholanesEubacterium: A genus of gram-positive, rod-shaped bacteria found in cavities of man and animals, animal and plant products, infections of soft tissue, and soil. Some species may be pathogenic. No endospores are produced. The genus Eubacterium should not be confused with EUBACTERIA, one of the three domains of life.Cholestasis: Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).Dehydrocholic Acid: A semisynthetic bile acid made from cholic acid. It is used as a cholagogue, hydrocholeretic, diuretic, and as a diagnostic aid.Cholestanetriol 26-Monooxygenase: An NAPH-dependent cytochrome P450 enzyme that catalyzes the oxidation of the side chain of sterol intermediates such as the 27-hydroxylation of 5-beta-cholestane-3-alpha,7-alpha,12-alpha-triol.Feces: Excrement from the INTESTINES, containing unabsorbed solids, waste products, secretions, and BACTERIA of the DIGESTIVE SYSTEM.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Cholecystography: Radiography of the gallbladder after ingestion of a contrast medium.Cholestyramine Resin: A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.Chromatography, Gas: Fractionation of a vaporized sample as a consequence of partition between a mobile gaseous phase and a stationary phase held in a column. Two types are gas-solid chromatography, where the fixed phase is a solid, and gas-liquid, in which the stationary phase is a nonvolatile liquid supported on an inert solid matrix.Receptors, Cytoplasmic and Nuclear: Intracellular receptors that can be found in the cytoplasm or in the nucleus. They bind to extracellular signaling molecules that migrate through or are transported across the CELL MEMBRANE. Many members of this class of receptors occur in the cytoplasm and are transported to the CELL NUCLEUS upon ligand-binding where they signal via DNA-binding and transcription regulation. Also included in this category are receptors found on INTRACELLULAR MEMBRANES that act via mechanisms similar to CELL SURFACE RECEPTORS.Gastrointestinal Agents: Drugs used for their effects on the gastrointestinal system, as to control gastric acidity, regulate gastrointestinal motility and water flow, and improve digestion.Taurine: A conditionally essential nutrient, important during mammalian development. It is present in milk but is isolated mostly from ox bile and strongly conjugates bile acids.Chromatography, Thin Layer: Chromatography on thin layers of adsorbents rather than in columns. The adsorbent can be alumina, silica gel, silicates, charcoals, or cellulose. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Hydroxycholesterols: Cholesterol which is substituted by a hydroxy group in any position.Mesocricetus: A genus of the family Muridae having three species. The present domesticated strains were developed from individuals brought from Syria. They are widely used in biomedical research.Cholecystectomy: Surgical removal of the GALLBLADDER.Biliary Fistula: Abnormal passage in any organ of the biliary tract or between biliary organs and other organs.Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alterations may be divided into METABOLIC DETOXICATION, PHASE I and METABOLIC DETOXICATION, PHASE II.Microsomes, Liver: Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.Sitosterols: A family of sterols commonly found in plants and plant oils. Alpha-, beta-, and gamma-isomers have been characterized.Carbadox: An antibacterial agent that has been used in veterinary practice for treating swine dysentery and enteritis and for promoting growth. However, its use has been prohibited in the UK following reports of carcinogenicity and mutagenicity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p125)Isoxazoles: Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.Lipid Metabolism, Inborn Errors: Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.Carbon Radioisotopes: Unstable isotopes of carbon that decay or disintegrate emitting radiation. C atoms with atomic weights 10, 11, and 14-16 are radioactive carbon isotopes.Kinetics: The rate dynamics in chemical or physical systems.Clostridium: A genus of motile or nonmotile gram-positive bacteria of the family Clostridiaceae. Many species have been identified with some being pathogenic. They occur in water, soil, and in the intestinal tract of humans and lower animals.Hydroxylation: Placing of a hydroxyl group on a compound in a position where one did not exist before. (Stedman, 26th ed)Chemistry: A basic science concerned with the composition, structure, and properties of matter; and the reactions that occur between substances and the associated energy exchange.Chemical Phenomena: The composition, conformation, and properties of atoms and molecules, and their reaction and interaction processes.Cholesterol, Dietary: Cholesterol present in food, especially in animal products.Hyperlipidemias: Conditions with excess LIPIDS in the blood.Hydroxymethylglutaryl CoA Reductases: Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.TritiumChromatography, High Pressure Liquid: Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.Lipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Isotope Labeling: Techniques for labeling a substance with a stable or radioactive isotope. It is not used for articles involving labeled substances unless the methods of labeling are substantively discussed. Tracers that may be labeled include chemical substances, cells, or microorganisms.

Sulphated and unsulphated bile acids in serum, bile, and urine of patients with cholestasis. (1/469)

Samples of serum, bile, and urine were collected simultaneously from patients with cholestasis of varying aetiology and from patients with cirrhosis; their bile acid composition was determined by gas/liquid chromatography and mass spectrometry. In cholestasis, the patterns in all three body fluids differed consistently and strikingly. In serum, cholic acid was the major bile acid and most bile acids (greater than 93%) were unsulphated, whereas, in urine, chenodeoxycholic was the major bile acid, and the majority of bile acids (greater than 60%) were sulphated. Secondary bile acids were virtually absent in bile, serum, and urine. The total amount of bile acids excreted for 24 hours correlated highly with the concentration of serum bile acids; in patients with complete obstruction, urinary excretion averaged 71-6 mg/24 h. In cirrhotic patients, serum bile acids were less raised, and chenodeoxycholic acid was the predominant acid. In healthy controls, serum bile acids were consistently richer in chenodeoxycholic acid than biliary bile acids, and no bile acids were present in urine. No unusual monohydroxy bile acids were present in patients with primary biliary cirrhosis, but, in several patients, there was a considerable amount of hyocholic acid present in the urinary bile acids. The analyses of individual bile acids in serum and urine did not appear to provide helpful information in the differential diagnosis of cholestasis. Thus, in cholestasis, conjugation of chenodeoxycholic acid with sulphate becomes a major biochemical pathway, urine becomes a major route of bile acid excretion, and abnormal bile acids are formed.  (+info)

Administration of an unconjugated bile acid increases duodenal tumors in a murine model of familial adenomatous polyposis. (2/469)

Intestinal carcinogenesis involves the successive accumulation of multiple genetic defects until cellular transformation to an invasive phenotype occurs. This process is modulated by many epigenetic factors. Unconjugated bile acids are tumor promoters whose presence in intestinal tissues is regulated by dietary factors. We studied the role of the unconjugated bile acid, chenodeoxycholate, in an animal model of familial adenomatous polyposis. Mice susceptible to intestinal tumors as a result of a germline mutation in Apc (Min/+ mice) were given a 10 week dietary treatment with 0.5% chenodeoxycholate. Following this, the mice were examined to determine tumor number, enterocyte proliferation, apoptosis and beta-catenin expression. Intestinal tissue prostaglandin E2 (PGE2) levels were also assessed. Administration of chenodeoxycholate in the diet increased duodenal tumor number in Min/+ mice. Promotion of duodenal tumor formation was accompanied by increased beta-catenin expression in duodenal cells, as well as increased PGE2 in duodenal tissue. These data suggest that unconjugated bile acids contribute to periampullary tumor formation in the setting of an Apc mutation.  (+info)

PhoP-PhoQ-regulated loci are required for enhanced bile resistance in Salmonella spp. (3/469)

As enteric pathogens, Salmonella spp. are resistant to the actions of bile. Salmonella typhimurium and Salmonella typhi strains were examined to better define the bile resistance phenotype. The MICs of bile for wild-type S. typhimurium and S. typhi were 18 and 12%, respectively, and pretreatment of log-phase S. typhimurium with 15% bile dramatically increased bile resistance. Mutant strains of S. typhimurium and S. typhi lacking the virulence regulator PhoP-PhoQ were killed at significantly lower bile concentrations than wild-type strains, while strains with constitutively active PhoP were able to survive prolonged incubation with bile at concentrations of >60%. PhoP-PhoQ was shown to mediate resistance specifically to the bile components deoxycholate and conjugated forms of chenodeoxycholate, and the protective effect was not generalized to other membrane-active agents. Growth of both S. typhimurium and S. typhi in bile and in deoxycholate resulted in the induction or repression of a number of proteins, many of which appeared identical to PhoP-PhoQ-activated or -repressed products. The PhoP-PhoQ regulon was not induced by bile, nor did any of the 21 PhoP-activated or -repressed genes tested play a role in bile resistance. However, of the PhoP-activated or -repressed genes tested, two (prgC and prgH) were transcriptionally repressed by bile in the medium independent of PhoP-PhoQ. These data suggest that salmonellae can sense and respond to bile to increase resistance and that this response likely includes proteins that are members of the PhoP regulon. These bile- and PhoP-PhoQ-regulated products may play an important role in the survival of Salmonella spp. in the intestine or gallbladder.  (+info)

The effect of bile salts and calcium on isolated rat liver mitochondria. (4/469)

Intact mitochondria were incubated with and without calcium in solutions of chenodeoxycholate, ursodeoxycholate, or their conjugates. Glutamate dehydrogenase, protein and phospholipid release were measured. Alterations in membrane and organelle structure were investigated by electron paramagnetic resonance spectroscopy. Chenodeoxycholate enhanced enzyme liberation, solubilized protein and phospholipid, and increased protein spin label mobility and the polarity of the hydrophobic membrane interior, whereas ursodeoxycholate and its conjugates did not damage mitochondria. Preincubation with ursodeoxycholate or its conjugate tauroursodeoxycholate for 20 min partially prevented damage by chenodeoxycholate. Extended preincubation even with 1 mM ursodeoxycholate could no longer prevent structural damage. Calcium (from 0.01 mM upward) augmented the damaging effect of chenodeoxycholate (0.15-0.5 mM). The combined action of 0.01 mM calcium and 0.15 mM chenodeoxycholate was reversed by ursodeoxycholate only, not by its conjugates tauroursodeoxycholate and glycoursodeoxycholate. In conclusion, ursodeoxycholate partially prevents chenodeoxycholate-induced glutamate dehydrogenase release from liver cell mitochondria by membrane stabilization. This holds for shorter times and at concentrations below 0.5 mM only, indicating that the different constitution of protein-rich mitochondrial membranes does not allow optimal stabilization such as has been seen in phospholipid- and cholesterol-rich hepatocyte cell membranes, investigated previously.  (+info)

Curcumin inhibits cyclooxygenase-2 transcription in bile acid- and phorbol ester-treated human gastrointestinal epithelial cells. (5/469)

We investigated whether curcumin, a chemopreventive agent, inhibited chenodeoxycholate (CD)- or phorbol ester (PMA)-mediated induction of cyclooxygenase-2 (COX-2) in several gastrointestinal cell lines (SK-GT-4, SCC450, IEC-18 and HCA-7). Treatment with curcumin suppressed CD- and PMA-mediated induction of COX-2 protein and synthesis of prostaglandin E2. Curcumin also suppressed the induction of COX-2 mRNA by CD and PMA. Nuclear run-offs revealed increased rates of COX-2 transcription after treatment with CD or PMA and these effects were inhibited by curcumin. Treatment with CD or PMA increased binding of AP-1 to DNA. This effect was also blocked by curcumin. In addition to the above effects on gene expression, we found that curcumin directly inhibited the activity of COX-2. These data provide new insights into the anticancer properties of curcumin.  (+info)

Antilithiasic effect of beta-cyclodextrin in LPN hamster: comparison with cholestyramine. (6/469)

Beta-Cyclodextrin (BCD), a cyclic oligosaccharide that binds cholesterol and bile acids in vitro, has been previously shown to be an effective plasma cholesterol lowering agent in hamsters and domestic pigs. This study examined the effects of BCD as compared with cholestyramine on cholesterol and bile acid metabolism in the LPN hamster model model for cholesterol gallstones. The incidence of cholesterol gallstones was 65% in LPN hamsters fed the lithogenic diet, but decreased linearly with increasing amounts of BCD in the diet to be nil at a dose of 10% BCD. In gallbladder bile, cholesterol, phospholipid and chenodeoxycholate concentrations, hydrophobic and lithogenic indices were all significantly decreased by 10% BCD. Increases in bile acid synthesis (+110%), sterol 27-hydroxylase activity (+106%), and biliary cholate secretion (+140%) were also observed, whereas the biliary secretion of chenodeoxycholate decreased (-43%). The fecal output of chenodeoxycholate and cholate (plus derivatives) was increased by +147 and +64%, respectively, suggesting that BCD reduced the chenodeoxycholate intestinal absorption preferentially. Dietary cholestyramine decreased biliary bile acid concentration and secretion, but dramatically increased the fecal excretion of chenodeoxycholate and cholate plus their derivatives (+328 and +1940%, respectively). In contrast to BCD, the resin increased the lithogenic index in bile, induced black gallstones in 34% of hamsters, and stimulated markedly the activities of HMG-CoA reductase (+670%), sterol 27-hydroxylase (+310%), and cholesterol 7alpha-hydroxylase (+390%). Thus, beta-cyclodextrin (BCD) prevented cholesterol gallstone formation by decreasing specifically the reabsorption of chenodeoxycholate, stimulating its biosynthesis and favoring its fecal elimination. BCD had a milder effect on lipid metabolism than cholestyramine and does not predispose animals to black gallstones as cholestyramine does in this animal model.  (+info)

Identification of a nuclear receptor for bile acids. (7/469)

Bile acids are essential for the solubilization and transport of dietary lipids and are the major products of cholesterol catabolism. Results presented here show that bile acids are physiological ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. When bound to bile acids, FXR repressed transcription of the gene encoding cholesterol 7alpha-hydroxylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding intestinal bile acid-binding protein, which is a candidate bile acid transporter. These results demonstrate a mechanism by which bile acids transcriptionally regulate their biosynthesis and enterohepatic transport.  (+info)

Bile acids: natural ligands for an orphan nuclear receptor. (8/469)

Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.  (+info)

Bile acid synthesis, determined by conversion of [4-14C]cholesterol into bile acids in rat and human hepatocytes and by measurement of mass production of bile acids in rat hepatocytes, was dose-dependently decreased by cyclosporin A, with 52% (rat) and 45% (human) inhibition of 10 microM. The decreased bile acid production in rat hepatocytes was due only to a fall in the synthesis of beta-muricholic and chenodeoxycholic acids (-64% at 10 microM-cyclosporin A), with no change in the formation of cholic acid. In isolated rat liver mitochondria, 26-hydroxylation of cholesterol was potently inhibited by the drug (concn. giving half-maximal inhibition = 4 microM). These results suggest that cyclosporin A blocks the alternative pathway in bile acid synthesis, which leads preferentially to the formation of chenodeoxycholic acid. ...
Bile acid in the stomach plays a key role in the digestion of food in the small intestine. Two chief bile acids produced in the body include chenodeoxycholic acid and cholic acid. These acids assist in the creation of micelles, which aids in breaking down dietary fat, and is integral for the digestion of fat in the small intestine. Bile acid is a fluid secreted by the hepatocytes that flows into the canaliculi. From the canaliculi, it reaches the bile ducts, and is then transferred to the gall bladder where it is concentrated with time and the addition of other bodily fluids. Bile acids are derived from the cholesterol inside of the hepatocytem, and are made up of hydrophilic or polar faces and lipid or hydrophobic faces. Cholesterol gets converted into chenodeoxycholic and cholic acids, which are two forms of bile acid. These are combined with amino acids and released into the canaliculi. This combined nature of bile acids enables them to perform two of the most important functions in the ...
PROTOCOL OUTLINE: Patients receive oral cholic acid and oral chenodeoxycholic acid on day 1. On day 4, patients receive oral cholic and ursodeoxycholic acids. Patients are assessed at 3 and 6 months for liver function response, neurologic status, and nutritional status.. Patients receive treatment until disease progression or unacceptable toxic effects are observed.. Completion date provided represents the completion date of the grant per OOPD records ...
For a long time, bilirubin (BR) has been considered a waste molecule with potential toxic effects especially on the central nervous system. Later, it was found that BR exhibited cytoprotective effects and mildly elevated BR levels showed antioxidant, anti-inflammatory and immunomodulatory properties, however, exact mechanisms of the anti-inflammatory actions of BR have not been fully understood yet. The main aim of this study was to assess the protective effects of BR using experimental in vivo and in vitro models in relation to inflammation and oxidative stress. Partial goal was to establish validated analytical method for determination of BR and lumirubin. Gunn and heterozygous rats were treated with lipopolysaccharide (LPS, 6 mg/kg, IP) or vehicle (saline). After 12 hours, blood and organs were collected for analyses of inflammatory and hepatic injury markers. Primary rat hepatocytes were treated with BR and TNF-α, HepG2 and SH-SY5Y cell lines were treated with BR and chenodeoxycholic acid. ...
Kit Component:- KN302990G1, Cdca3 gRNA vector 1 in pCas-Guide vector- KN302990G2, Cdca3 gRNA vector 2 in pCas-Guide vector- KN302990D, donor vector…
1. The duodenal bile acid composition was analysed in 24 control subjects and 107 patients with various types of hyperlipoproteinaemia. A highly significant negative correlation was observed between the proportions of deoxycholic acid and cholic acid as well as between deoxycholic acid and chenodeoxycholic acid. Patients with gall-bladder disease had an increased proportion of deoxycholic acid in their bile.. 2. Eight control subjects were studied before and during the ingestion of 1·9 mmol (0·75 g) of deoxycholic acid daily. In these subjects a rise in the proportion of deoxycholic acid was also accompanied by a fall in the proportion of both cholic acid and chenodeoxycholic acid in duodenal bile.. 3. The biliary lipid composition and cholesterol saturation was determined before and during the administration of 1·9 mmol (0·75 g) of chenodeoxycholic acid (n = 12) or deoxycholic acid (n = 8) daily for 3-4 weeks. The cholesterol saturation was decreased during the chenodeoxycholic acid ...
Cholelithiasis (gallstones) is a major medical and economic problem in the USA (Schoenfield, 1977; Schoenfield et al., 1981). It has been estimated to have a prevalence of 15 million women and five...
Xing, X., Burgermeister, E., Geisler, F., Einwächter, H., Fan, L., Hiber, M., Rauser, S., Walch, A., Röcken, C., Ebeling, M., Wright, M. B., Schmid, R. M. and Ebert, M. P.A. (2009), Hematopoietically expressed homeobox is a target gene of farnesoid X receptor in chenodeoxycholic acid-induced liver hypertrophy. Hepatology, 49: 979-988. doi: 10.1002/hep.22712 ...
FXR is expressed at high levels in the liver and intestine. Chenodeoxycholic acid and other bile acids are natural ligands for FXR. Similar to other nuclear receptors, when activated, FXR translocates to the cell nucleus, forms a dimer (in this case a heterodimer with RXR) and binds to hormone response elements on DNA, which up- or down-regulates the expression of certain genes.[6] One of the primary functions of FXR activation is the suppression of cholesterol 7 alpha-hydroxylase (CYP7A1), the rate-limiting enzyme in bile acid synthesis from cholesterol. FXR does not directly bind to the CYP7A1 promoter. Rather, FXR induces expression of small heterodimer partner (SHP), which then functions to inhibit transcription of the CYP7A1 gene. In this way, a negative feedback pathway is established in which synthesis of bile acids is inhibited when cellular levels are already high. FXR has also been found to be important in regulation of hepatic triglyceride levels.[7] Studies have also shown the FXR to ...
Before the biochemical basis of SLO syndrome was understood, it was well recognised that a significant proportion of infants with SLO syndrome had a major feeding problem associated with marked failure to thrive and irritability. Some of these infants showed an improvement in weight gain when the calorie density of their feeds was increased; others showed remarkable catch up weight gain after nasogastric or gastrostomy feeds were begun. When fed adequately, these infants were less irritable. The fact that such improvements can be achieved by correcting malnutrition must be borne in mind when assessing the results obtained with other dietary manipulations.. In 1994, Irons et al described the effects of supplementation with cholesterol (20-40 mg/kg/day), ursodeoxycholic acid (15 mg/kg/day), and chenodeoxycholic acid (7 mg/kg/day) in a 14 month old girl with SLO syndrome.31 There was a clear increase in the plasma cholesterol, but no fall in the plasma concentration of 7-dehydrocholesterol. Ullrich ...
Worldwide, metabolic diseases such as obesity and type 2 diabetes have reached epidemic proportions. A major regulator of metabolic processes that gained interest in recent years is the bile acid receptor TGR5 (Takeda G protein-coupled receptor 5). This G protein-coupled membrane receptor can be found predominantly in the intestine, where it is mainly responsible for the secretion of the incretins glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). The aim of this study was (i) to identify plant extracts with TGR5-activating potential, (ii) to narrow down their activity to the responsible constituents, and (iii) to assess whether the intestinal microbiota produces transformed metabolites with a different activity profile. Chenodeoxycholic acid (CDCA) served as positive control for both, the applied cell-based luciferase reporter gene assay for TGR5 activity and the biotransformation assay using mouse fecal slurry. The suitability of the workflow was demonstrated by the biotransformation of ...
Worldwide, metabolic diseases such as obesity and type 2 diabetes have reached epidemic proportions. A major regulator of metabolic processes that gained interest in recent years is the bile acid receptor TGR5 (Takeda G protein-coupled receptor 5). This G protein-coupled membrane receptor can be found predominantly in the intestine, where it is mainly responsible for the secretion of the incretins glucagon-like peptide 1 (GLP-1) and peptide YY (PYY). The aim of this study was (i) to identify plant extracts with TGR5-activating potential, (ii) to narrow down their activity to the responsible constituents, and (iii) to assess whether the intestinal microbiota produces transformed metabolites with a different activity profile. Chenodeoxycholic acid (CDCA) served as positive control for both, the applied cell-based luciferase reporter gene assay for TGR5 activity and the biotransformation assay using mouse fecal slurry. The suitability of the workflow was demonstrated by the biotransformation of ...
Rabbit polyclonal Borealin/CDCA8 antibody validated for WB and tested in Human, Mouse and Rat. With 1 independent review. Immunogen corresponding to synthetic…
Bile acid diarrhoea (BAD) is an under-recognised but common condition of chronic watery diarrhoea. BAD may be secondary to ileal disease affecting the reabsorption and the enterohepatic circulation of bile acids (bile acid malabsorption) or can be an idiopathic, primary BAD (PBAD). In work published in 2009, we described a new mechanism to explain this syndrome of primary BAD.. Blood levels of the hormone fibroblast growth factor 19 (FGF19) are reduced in primary and secondary BAD, producing impaired feedback inhibition of bile acid synthesis, leading to excess faecal bile acids, which then produce diarrhoea by stimulating colonic secretion. FGF19 is synthesised in the ileum and we have shown transcription is markedly induced by farnesoid X receptor(FXR) agonists such as chenodeoxycholic acid, an abundant natural bile acid. More potent FXR agonists are logical diagnostic and therapeutic agents for this condition, and obeticholic acid (OCA), which is 100x more potent than chenodeoxycholic acid, ...
Involved in bile acid metabolism. In liver hepatocytes catalyzes the second step in the conjugation of C24 bile acids (choloneates) to glycine and taurine before excretion into bile canaliculi. The major components of bile are cholic acid and chenodeoxycholic acid. In a first step the bile acids are converted to an acyl-CoA thioester, either in peroxisomes (primary bile acids deriving from the cholesterol pathway), or cytoplasmic at the endoplasmic reticulum (secondary bile acids). May catalyze the conjugation of primary or secondary bile acids, or both. The conjugation increases the detergent properties of bile acids in the intestine, which facilitates lipid and fat-soluble vitamin absorption. In turn, bile acids are deconjugated by bacteria in the intestine and are recycled back to the liver for reconjugation (secondary bile acids). May also act as an acyl-CoA thioesterase that regulates intracellular levels of free fatty acids. In vitro, catalyzes the hydrolysis of long- and very long-chain ...
Involved in bile acid metabolism. In liver hepatocytes catalyzes the second step in the conjugation of C24 bile acids (choloneates) to glycine and taurine before excretion into bile canaliculi. The major components of bile are cholic acid and chenodeoxycholic acid. In a first step the bile acids are converted to an acyl-CoA thioester, either in peroxisomes (primary bile acids deriving from the cholesterol pathway), or cytoplasmic at the endoplasmic reticulum (secondary bile acids). May catalyze the conjugation of primary or secondary bile acids, or both. The conjugation increases the detergent properties of bile acids in the intestine, which facilitates lipid and fat-soluble vitamin absorption. In turn, bile acids are deconjugated by bacteria in the intestine and are recycled back to the liver for reconjugation (secondary bile acids). May also act as an acyl-CoA thioesterase that regulates intracellular levels of free fatty acids. In vitro, catalyzes the hydrolysis of long- and very long-chain ...
Dihydroxy bile acids, such as chenodeoxycholic acid (CDCA), are well known to promote colonic fluid and electrolyte secretion, thereby causing diarrhoea associated with bile acid malabsorption. However, CDCA is rapidly metabolised by colonic bacteria to ursodeoxycholic acid (UDCA), the effects of which on epithelial transport are poorly characterised. Here, we investigated the role of UDCA in the regulation of colonic epithelial secretion. Cl(-) secretion was measured across voltage-clamped monolayers of T84 cells and muscle-stripped sections of mouse or human colon. Cell surface biotinylation was used to assess abundance/surface expression of transport proteins. Acute (15 min) treatment of T84 cells with bilateral UDCA attenuated Cl(-) secretory responses to the Ca(2+) and cAMP-dependent secretagogues carbachol (CCh) and forskolin (FSK) to 14.0 ± 3.8 and 40.2 ± 7.4% of controls, respectively (n = 18, P , 0.001). Investigation of the molecular targets involved revealed that UDCA acts by ...
An epimer of Chenodeoxycholic Acid. It is a mammalian Bile acid found first in the Bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of Bile and may dissolve Gallstones. It is used as a cholagogue and choleretic ...
1433 Colorectal cancer (CRC) is the second leading cause of cancer death in the United States. Secondary bile acids (BA), in particular deoxycholic acid (DCA), promote colorectal adenomas (CRA) and CRC. Ursodeoxycholic acid (UDCA), the 7Β-epimer of chenodeoxycholic acid, has been shown to inhibit colorectal carcinogenesis in animal models and in individuals at increased risk of CRC. The precise mechanisms by which UDCA prevents CRC are unknown, but one potential mechanism is that UDCA alters the bile acid profile and reduces exposure of the colorectum to harmful effects of secondary BAs. We previously published results of a phase III trial of UDCA on CRA recurrence in 1285 subjects. The major findings were a non-significant 12% reduction in adenoma recurrence and a significant 39% reduction (p=0.03) in recurrence of adenomas with high-grade dysplasia (HGD). As part of this study we collected 72-hr fecal and plasma samples for BA analysis at baseline and 3 years of intervention on a subset of ...
Obeticholic acid (abbreviated to OCA, trade name Ocaliva), is a semi-synthetic bile acid analogue which has the chemical structure 6α-ethyl-chenodeoxycholic acid. It is used as a drug to treat primary biliary cholangitis, and is undergoing development for several other liver diseases and related disorders. Intercept Pharmaceuticals Inc. hold the worldwide rights to develop OCA outside Japan and China, where it is licensed to Dainippon Sumitomo Pharma. The natural bile acid, chenodeoxycholic acid, was identified in 1999 as the most active physiological ligand for the farnesoid X receptor (FXR), which is involved in many physiological and pathological processes. A series of alkylated bile acid analogues were designed, studied and patented by Roberto Pellicciari and colleagues at the University of Perugia, with 6α-ethyl-chenodeoxycholic acid emerging as the most highly potent FXR agonist. FXR-dependent processes in liver and intestine were proposed as therapeutic targets in human diseases. ...
The diethanolamine salt of the mono (α,p-dimethylbenzyl) ester of d-camphoric acid (Gallogen) augmented diet-induced hypercholesterolemia and hyperlipemia in the rat, while depressing liver cholesterol and total lipid concentrations. Diethanolamine had virtually identical effects. Gallogen, given orally to rats with biliary fistulas had a slight hydrocholeretic effect, but did not influence biliary excretion of cholesterol, cholic acid, or chenodeoxycholic acid.. ...
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Illustration of a Lithocholic Acid molecular model. Recent research has shown that lithocholic acid (LCA), which is naturally produced in the liver during digestion, can kill several types of cancer cells, including those found in some brain tumours and breast cancer. Key: black=carbon, white=hydrogen, red=oxygen. - Stock Image C022/4469
Complete information for CDCA8 gene (Protein Coding), Cell Division Cycle Associated 8, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Faecal bile acid excretion and intestinal transit time were studied in 18 children with inflammatory bowel disease in clinical remission and with normal stools: 16 with ulcerative colitis, two with Crohns colitis, mean age 14 years (range 10-17 years). Five healthy children, mean age 12.4 years (range 10-17 years), were studied as control subjects. Most patients were taking sulphasalazine, but none were taking steroids. Transit time was determined by carmine and did not differ between groups. Faeces were collected for 72 hours, and faecal water was prepared by centrifugation of faeces at 15,000 x g for two hours. Bile acids in total faeces and faecal water were studied using capillary gas-liquid chromatography-mass spectrometry. Faecal excretion of total bile acids, unconjugated bile acids, and glycine and taurine conjugates were significantly increased in patients as was faecal water excretion of total bile acids, particularly the taurine conjugates and cholic and chenodeoxycholic acids. Total ...
Dec 22, 2005. SAN DIEGO, CA - Dec 22, 2005 - Diazyme Laboratories, a company that applies its proprietary enzyme technologies to develop low cost and high quality diagnostic products for clinical and research uses, announced today that the U.S. Food and Drug Administration (FDA) has granted Diazyme 510(K) clearance to market its Enzymatic Total Bile Acids (TBA) Assay Kit for the quantitative determination of total bile acids in human blood samples.. Total bile acids is a well known bio-marker for diagnosis of liver diseases. Serum total bile acids are elevated in patients with acute hepatitis, chronic hepatitis, liver sclerosis, and liver cancer. Total bile acids levels are found to be the most sensitive indicator for monitoring the effectiveness of interferon treatment of chronic hepatitis C patients. Moreover, total bile acids tests are also widely used to screen pregnant women for the condition of obstetric cholestasis, a disease that is caused by elevated total bile acids in the bloodstream ...
To determine the optimum bile acid regimen for rapid gall stone dissolution, 48 gall stone patients were divided into four groups of 12 according to stone diameter and were randomly allocated to receive one of four treatment regimens: bedtime or mealtime chenodeoxycholic acid (CDCA, 12 mg/kg/day) and bedtime or mealtime ursodeoxycholic acid (UDCA, 12 mg/kg/day). An additional 10 patients treated with a combination of CDCA plus UDCA (each 6 mg/kg/day) at bedtime were matched with the 10 patients on bedtime CDCA and the 10 on bedtime UDCA. The gall stone dissolution rates at six and 12 months were determined by standardised oral cholecystography and expressed as the percentage reduction in the gall stone volume after treatment. The gall stone dissolution rate at six months was higher for UDCA than CDCA treatment (median 78% v 48%, p less than 0.01), and for bedtime than mealtime administration (69% v 39%, p less than 0.02). Both differences were greater for stones less than 8 mm diameter. The ...
BACKGROUND & AIMS: Oral administration of ursodeoxycholic acid (UDCA) and cholesterol causes bile salt malabsorption; the former by competition for and the latter by down-regulation of ileal bile acid transporters. Because ileectomy in rats induces enterohepatic cycling of bilirubin, the hypothesis that dietary steroids might have the same effect was tested. METHODS: Male inbred C57L/J mice and Sprague-Dawley rats were fed low doses of UDCA, chenodeoxycholic acid (CDCA), or cholesterol added to laboratory chow with simultaneous chow-fed controls. After 1 week (mice) or 2 weeks (rats), indices of bile salt malabsorption and enterohepatic cycling of bilirubin were measured, including bilirubin secretion rates into bile, serum and intestinal bilirubin and bile salt levels, and urobilinogen levels in cecum, large intestine, and feces. RESULTS: Dietary UDCA and cholesterol, but not CDCA, significantly increased bilirubin secretion rates into bile. In UDCA-fed mice, gallbladder biles contained
Anhui Chem-Bright Bioengineering Co.,Ltd is a modernized enterprise specialized in research & development, manufacturing and selling of Active Pharmaceutical Intermediates and feed additive.. Our main products are cholesterol, bilirubin,cholic acid, hyodeoxycholic acid, chenodeoxycholic acid, pig bile powder, ox bile powder,sodium cholate,Deoxycholic acid,Sodium Deoxycholate,Dehydrocholic acid,Sodium Dehydrocholate,Chondronitin Sulfate.. Our factory covers an area of over 36,000 square meter, included standard workshop, warehouse, research center, laboratory, office building, and other devices, with a total investment of more than CNY 75 million.We had established 10-thousand-grade Purification Room, and introduced advanced equipments both for research and production from home and abroad. Our production management is strictly conducted by the requirement of GMP of China,ISO9001-2008, and all of our products could meet the requirements of international standards.In 2013, products including ...
Abstract Recent studies indicate an important role for nuclear receptors in regulating lipid and carbohydrate metabolism, fibrosis and inflammation. Farnesoid X receptor (FXR) is a member of the nuclear hormone receptor superfamily. FXR is highly expressed in the liver, intestine, adrenal gland and kidney. The primary bile acids are the highest affinity endogenous ligands for FXR. The effects of FXR agonists in diabetic kidney disease, the main cause of end stage renal disease, however have not been determined. To identify the effect of FXR activation in modulation of diabetic nephropathy, we have treated 1) C57BL/6J mice on low fat diet or high fat diet with FXR agonists (GW4064 or cholic acid) for one week; 2) C57BLKS/J-db/db mice and their lean mates with GW4064 for one week; and 3) C57BL/6J-db/db mice and their lean mates with cholic acid for 12 weeks. We found that FXR agonists modulate renal SREBP-1 expression and lipid metabolism, as well as renal expression of profibrotic growth factors, ...
UDCA (ursodeoxycholic acid) is used increasingly for the treatment of cholestatic liver diseases. Among other cytoprotective effects, this endogenous bile acid is a potent inhibitor of apoptosis, interfering with both intrinsic and extrinsic apoptotic pathways. In previous studies, we have demonstrated that the transforming growth factor β1-induced E2F-1/Mdm2 (murine double minute 2)/p53 apoptotic pathway was an upstream molecular target of UDCA. In agreement with this, we have recently established p53 as a key molecular target in UDCA prevention of cell death. The tumour suppressor p53 is a well-described transcription factor that induces the expression of multiple different pro-apoptotic gene products. Its regulation involves a variety of signalling proteins and small molecules, and occurs at multiple levels, including transcription, translation and post-translation levels. In the present study, by using different biophysical techniques, we have investigated the possibility of a direct ...
The results of the preliminary test showed that less than 50% of the test item has been hydrolysed in 2.4 hours at, and that less than 10% of the test item has been hydrolysed after five days for the three pH values, the full test was not performed. Therefore, according to guideline dispositions, the full test was not performed and it can be concluded that the abiotic degradation hydrolysis of ursodeoxycholic acid is lower than 10% after 5 days atfor the pH values 4, 7 and 9. If released into the environment, ursodeoxycholic acid is not expected to hydrolyze. ...
This page contains information about Glucuronides of Ursodeoxycholic Acid 3-O-β-D-glucuronide. Purchase Ursodeoxycholic Acid 3-O-β-D-glucuronide online
The particle size distrubution of ursodeoxycholic acid has been analyzed according to method MT 187 and OECD guideline No. 110. The average percentile size for 10%, 50% and 90% of the sample were 1.31 µm, 14.4 µm and 57.3 µm, respectively. In the same study it can be concluded that 86.7% of the test item presents a particle size lower than 50μm and 4.9% of test item was found above 75μm. ...
/PRNewswire/ -- ReportsnReports adds present scenario (with the base year being 2017) and the growth prospects of global Ursodeoxycholic Acid market for...
The primary bile acids (BAs) are synthetized from colesterol in the liver, conjugated to glycine or taurine to increase their solubility, secreted into bile, concentrated in the gallbladder during fasting, and expelled in the intestine in response to dietary fat, as well as bio-transformed in the colon to the secondary BAs by the gut microbiota, reabsorbed in the ileum and colon back to the liver, and minimally lost in the feces. BAs in the intestine not only regulate the digestion and absorption of cholesterol, triglycerides, and fat-soluble vitamins, but also play a key role as signaling molecules in modulating epithelial cell proliferation, gene expression, and lipid and glucose metabolism by activating farnesoid X receptor (FXR) and G-protein-coupled bile acid receptor-1 (GPBAR-1, also known as TGR5) in the liver, intestine, muscle and brown adipose tissue ...
Creative-Proteomics offer cas 83-44-3 DEOXYCHOLIC ACID (2,2,4,4-D4, 98%). We are specialized in manufacturing Stabel Isotope Labeled Analytical Standard products.
To find out which is the best solution for dark circles under your eyes, consult with an ophthalmologist. Remember that surgery alone will not be the complete solution for the complete dissolution of dark circles. If you continue with an unhealthy lifestyle, the dark circles under your eyes may reappear again. It is also important to stick to a strict skin care regimen. Always wear sunscreen, especially when you are going out under the sun. Wearing sunglasses can be very helpful, too, to add extra protection for your thin under eye skin ...
Using deoxycholic acid as starting materials, a series of 12a-aza-C-homo-12-one 7-deoxycholic acid derivatives were synthesized The antiproliferative activity of the synthesized compounds against some carcinoma cell lines was investigated. The results showed that some 12-oxy-12a-aza-C-homo-7-deoxycholic acid derivatives displayed distinct cytotoxicity to HeLa (human cervical carcinoma) and Tu 686 (laryngocarcinoma) tumor ...
Sigma-Aldrich offers abstracts and full-text articles by [Halka Buryova, Karel Chalupsky, Olga Zbodakova, Ivan Kanchev, Marketa Jirouskova, Martin Gregor, Radislav Sedlacek].
Crystalline lithocholic (3α-hydroxycholanic) acid was isolated from a pooled sample of feces from healthy men for the first time. This acid, which occurs in small amounts in human bile, was obtained by alcohol extraction, followed by solvent partition and chromatography. Under these conditions most of the acid was recovered in the form of its methyl ester. ...
Recombinant human CDCA8 protein, fused to His-tag at N-terminus, was expressed in E.coli and purified by using conventional chromatography techniques (19-280aa).
The secondary bile acids are derived from the primary bile acids by the enzymatic action of intestinal bacteria through the process of deconjugation and dehydroxylation. The secondary bile acids in humans include deoxycholic acid and lithocholic acid, formed from the 7alpha-dehydroxylation of cholic acid and chenodeoxycholic acid, respectively ...
Gallstone Dissolution. On the basis of clinical trial results in a total of 868 patients with radiolucent gallstones treated in 8 studies (three in the U.S. involving 282 patients, one in the U.K. involving 130 patients, and four in Italy involving 456 patients) for periods ranging from 6-78 months with Ursodiol doses ranging from about 5 to 20 mg/kg/day, an Ursodiol dose of about 8-10 mg/kg/day appeared to be the best dose. With an Ursodiol dose of about 10 mg/kg/day, complete stone dissolution can be anticipated in about 30% of unselected patients with uncalcified gallstones , 20 mm in maximal diameter treated for up to 2 years. Patients with calcified gallstones prior to treatment, or patients who develop stone calcification or gallbladder nonvisualization on treatment, and patients with stones , 20 mm in maximal diameter rarely dissolve their stones. The chance of gallstone dissolution is increased up to 50% in patients with floating or floatable stones (i.e., those with high cholesterol ...
The serum concentration of TBA in healthy neonates significantly exceeds that in children over 1 year of age, a condition called physiological cholestasis.9 The urinary TBA:creatinine ratio was raised in the first week after birth, then decreased gradually. The high concentration of TBA in urine may be attributable to either an enhanced stimulation of the enterohepatic circulation of bile acids or an impaired hepatic clearance or excretion.10The highest value for TBA in meconium was in neonates. This value is greatly influenced by events or conditions during pregnancy, such as the presence of biliary bile in the fetal duodenum or the ingestion of amniotic fluid by the fetus.10 11 Ketonic bile acids are usually considered to result from the bacterial oxidation of primary bile acids.12 In this study we detected ketonic bile acids early in life. The intestine may be colonised by bacterial flora during the first week.13 A high concentration of 3-oxo Δ4 bile acids in serum or urine has been ...
View drug interactions between cholic acid and deoxycholic acid. These medicines may also interact with certain foods or diseases.
Hyperactivation of NF-κB is a key factor in the pathophysiology of inflammatory bowel disease (IBD). We previously showed that the bile salt nuclear Farnesoid X Receptor (FXR) counter-regulates intestinal inflammation, possibly via repression of NF-κB. Here, we examine whether mutual antagonism between NF-κB and FXR exists. FXR and its target genes IBABP and FGF15/19 expression were determined in HT29 colon carcinoma cells and ex vivo in intestinal specimens of wild type (WT) and Fxr-ko mice, treated with/without FXR ligands (GW4064/INT-747) and inflammatory stimuli (TNFα/IL-1β). In addition, FXR activation was studied in vivo in WT and Fxr-ko mice with DSS-colitis. The involvement of NF-κB in decreasing FXR activity was investigated by reporter assays and Glutathione S-transferase pulldown assays. FXR target gene expression was highly reduced by inflammatory stimuli in all model systems, while FXR mRNA expression was unaffected. In line with these results, reporter assays showed reduced ...
x] J Biol Chem. 2011 Aug 12;286(32):28382-95. Nutritional regulation of bile acid metabolism is associated with improved pathological characteristics of the metabolic syndrome. Liaset B, Hao Q, Jørgensen H, Hallenborg P, Du ZY, Ma T, Marschall HU, Kruhøffer M, Li R, Li Q, Yde CC, Criales G, Bertram HC, Mellgren G, Ofjord ES, Lock EJ, Espe M, Frøyland L, Madsen L, Kristiansen K. "Bile acids (BAs)3 are synthesized in the liver from cholesterol. After their synthesis, they are conjugated to the amino acids taurine or glycine in a species-dependent manner (1). Conjugation of bile acids increases their solubility and facilitates their secretion into bile (2). [...] the dietary levels of these amino acids might be crucial for BA conjugation and secretion [...] In conclusion, we provide compelling evidence that plasma bile acid levels can be modulated by the dietary protein source in high fat-treated rats. Increased levels of plasma BAs were associated with a significant reduction in diet-induced ...
Description: A bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent ...
Kybella (deoxycholic acid) is the first and only FDA-approved injectable treatment to improve the appearance of moderate to severe fat beneath the chin.
0039]A 200 ml three-necked flask having a thermometer, a condenser, and a stirrer was prepared. Then, 6.68 g (20 mmol) of 1,3,3-tris(4-hydroxyphenyl)butane and 25 ml of N-methyl-2-pyrrolidone were placed in the three-necked flask and stirred while being heated at 80° C. in an atmosphere of nitrogen until 1,3,3-tris(4-hydroxyphenyl)butane was completely dissolved in N-methyl-2-pyrrolidone. After complete dissolution, 23.46 g (72 mmol) of cesium carbonate was added thereto, and the resulting mixture was further stirred for 30 minutes. Then, 17.84 g (66 mmol) of 2-(3-oxetanyl)butyltosylate previously synthesized was added thereto, and the resulting mixture was stirred for 20 hours at 80° C. in an atmosphere of nitrogen. After the completion of reaction, the mixture was cooled to room temperature, and 100 ml of ethyl acetate and 50 ml of distilled water were added to the mixture. The resulting mixture was left standing to separate into an aqueous phase and an organic phase. The thus obtained ...
Order cheap Actigall, Ursofalk, Urso (Ursodiol) 150, 300, 600 mg from $1.12 per pill to treat and prevent gallstones, biliary cirrhosis, liver diseases.
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Bile Acid Factors™ consists of a mixture of highly concentrated bile acids (also called bile salts), mostly in the conjugated form, from U.S. and/or New Zealan
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The multifactorial mechanisms promoting weight loss and improved metabolism following Roux-en-Y gastric bypass (GB) surgery remain incompletely understood. Recent rodent studies suggest that bile acids can mediate energy homeostasis by activating the G-protein coupled receptor TGR5 and the type 2 thyroid hormone deiodinase. Altered gastrointestinal anatomy following GB could affect enterohepatic recirculation of bile acids. We assessed whether circulating bile acid concentrations differ in patients who previously underwent GB, which might then contribute to improved metabolic homeostasis. We performed cross-sectional analysis of fasting serum bile acid composition and both fasting and post-meal metabolic variables, in three subject groups: (i) post-GB surgery (n = 9), (ii) without GB matched to preoperative BMI of the index cohort (n = 5), and (iii) without GB matched to current BMI of the index cohort (n = 10). Total serum bile acid concentrations were higher in GB (8.90 +/- 4.84 micromol/l) than in
TY - JOUR. T1 - FTF and LRH-1, two related but different transcription factors in human Caco-2 cells. T2 - Their different roles in the regulation of bile acid transport. AU - Pan, Debra H.. AU - Chen, Frank. AU - Neimark, Ezequiel. AU - Li, Xiaoping. AU - Shneider, Benjamin L.. PY - 2005/12/30. Y1 - 2005/12/30. N2 - The apical sodium dependent bile acid transporter (ASBT) mediates ileal bile acid reabsorption. The transcription factors, liver receptor homologue-1 (LRH-1:mouse) and fetoprotein transcription factor (FTF:human), are presumably orthologues. Bile-acid induced negative feedback regulation of mouse (m) and human (h) ASBT occurs via LRH-1 and RAR/RXR, respectively. hASBT has a potential FTF cis-element, although its functional role is unknown. hASBT and mASBT promoter constructs and an FTF cis-element mutated hASBT (hASBT/FTFμ) were assessed in human Caco-2 cells treated with chenodeoxycholic acid (CDCA) and/or co-transfected with hFTF, mLRH-1, or specific small interfering FTF or ...
Since the last International Bile Acid Meeting in Freiburg in 1996, considerable progress has been made in several areas of bile acid research. The different pathways of bile acid synthesis and their regulation have been further characterized. The molecular mechanisms for biliary secretion of bile acids have been elucidated and genetic defects of bile acid transport have been defined. Injurious as well as protective effects of different bile acids on the liver have been further studied. Finally, the beneficial effects of ursodeoxycholic acid in cholestatic liver diseases have been substantiated and the potential mechanisms of action have been explored. This book, the proceedings of the Falk Symposium No. 108 (XV International Bile Acid Meeting), held in Titisee, Germany, October 12-13, 1998, is dedicated to both basic and clinical aspects of bile acid research with a focus on bile acids and cholestasis.Bile Acids and Cholestasis - XV International Bile Acid Meeting, 1 was published 1999 under ...
Porphyrin YD2-o-C8-based dyes were employed to sensitize room-temperature (RT) chemical-assembled ZnO aggregated anodes for use in dye-sensitized solar cells (DSSCs). To reduce the acidity of the YD2-o-C8 dye solution, the proton in the carboxyl group of a porphyrin dye was replaced with tetrabuthyl ammonium (TBA+) in this work. The short-circuit current density (Jsc) of the YD2-o-C8-TBA-sensitized ZnO DSSCs is higher than that of the YD2-o-C8-sensitized cells, resulting in the improvement of the efficiency of the YD2-o-C8-based ZnO DSSCs. With an appropriate incorporation of chenodeoxycholic acid (CDCA) as coadsorbate, the Jsc and efficiency of the YD2-o-C8-TBA-sensitized ZnO DSSC are enhanced due to the improvement of the incident-photon-to-current efficiency (IPCE) values in the wavelength range of 400-450 nm. Moreover, a considerable increase in Jsc is achieved by the addition of a light scattering layer in the YD2-o-C8-TBA-sensitized ZnO photoanodes. Significant IPCE enhancement in the range 475
To study the effect of steroid hormones on bile acid synthesis by cultured rat hepatocytes, cells were incubated with various amounts of these compounds during 72 h and conversion of [4-14C]cholesterol into bile acids was measured. Bile acid synthesis was stimulated in a dose-dependent way by glucocorticoids, but not by sex steroid hormones, pregnenolone or the mineralocorticoid aldosterone in concentrations up to 10 microM. Dexamethasone proved to be the most efficacious inducer, giving 3-fold and 7-fold increases in bile acid synthesis during the second and third 24 h incubation periods respectively, at a concentration of 50 nM. Mass production of bile acids as measured by g.l.c. during the second day of culture (28-52 h) was 2.2-fold enhanced by 1 microM-dexamethasone. No change in the ratio of bile acids produced was observed during this period in the presence of dexamethasone. Conversion of [4-14C]7 alpha-hydroxycholesterol, an intermediate of the bile acid pathway, to bile acids was not ...
Ursodeoxycholic acid (UDCA) is a non-toxic, hydrophilic bile acid in widespread clinical use mainly for acute and chronic liver disease. Recently, treatment with UDCA in hepatic graft-ver-sus-host dis
Manufacturer of Pharmaceutical Dry Syrups - Ursodeoxycholic Acid Oral Suspension offered by Myrra Lifecare (Division Of Stellar Biolabs), Chandigarh.
Cholic acid is a bile acid. Bile acids are produced naturally in the body to aid in digestion of fats and certain nutrients. People with bile acid disorders are unable to produce cholic acid normally. This can make it harder for the body to absorb nutrients important for health, growth, and body functioning. Abnormal...
Stolz, A., Sugiyama, Y., Kuhlenkamp, J., Osadchey, B., Yamada, T., Belknap, W., Balistreri, W. and Kaplowitz, N. (1986), Cytosolic bile acid binding protein in rat liver: Radioimmunoassay, molecular forms, developmental characteristics and organ distribution. Hepatology, 6: 433-439. doi: 10.1002/hep.1840060319 ...
x] J Biol Chem. 2011 Aug 12;286(32):28382-95. Nutritional regulation of bile acid metabolism is associated with improved pathological characteristics of the metabolic syndrome. Liaset B, Hao Q, Jørgensen H, Hallenborg P, Du ZY, Ma T, Marschall HU, Kruhøffer M, Li R, Li Q, Yde CC, Criales G, Bertram HC, Mellgren G, Ofjord ES, Lock EJ, Espe M, Frøyland L, Madsen L, Kristiansen K. "Bile acids (BAs)3 are synthesized in the liver from cholesterol. After their synthesis, they are conjugated to the amino acids taurine or glycine in a species-dependent manner (1). Conjugation of bile acids increases their solubility and facilitates their secretion into bile (2). [...] the dietary levels of these amino acids might be crucial for BA conjugation and secretion [...] In conclusion, we provide compelling evidence that plasma bile acid levels can be modulated by the dietary protein source in high fat-treated rats. Increased levels of plasma BAs were associated with a significant reduction in diet-induced ...
We have previously shown that SHP is a transcriptional repressor of CYP2D6 expression (Koh et al., 2014), and activation of the FXR and SHP pathways by using a synthetic FXR agonist leads to decreased CYP2D6 expression and activity (Pan et al., 2015). Bile acids are endogenous activators of FXR that are capable of upregulating SHP within hours (Fang et al., 2007; Miao et al., 2009); however, it remains unclear how chronically elevated concentrations of bile acids (e.g., in cholestatic conditions) affect SHP expression/activity and thus its regulation of CYP2D6 expression. In this study, we employed CA feeding in mice to mimic cholestatic conditions and unexpectedly found that CA feeding decreased SHP protein levels, thus increasing CYP2D6 expression and activity.. In this study, mRNA expression levels of SHP were similar between the control and CA-fed mice, but SHP protein expression was decreased upon CA feeding. The lack of SHP induction by bile acids was also observed in a previous study ...
ALT: 15,360 (rat normal 29-65). Contributors Diagnosis and Comments: Moderate to severe, acute, multifocal to coalescing centrilobular hepatic necrosis.. Acute coagulative necrosis of the centrilobular region (Zone 3 of the liver acinus) is present throughout this section of rat liver. The necrosis of hepatocytes is most severe in zone 3, with complete dissolution of cytoplasmic components, karyorrhexis and karyolysis, and breakdown of sinusoidal endothelium with blood-filled lakes in the immediate vicinity of central veins. Phagocytosis by large cells assumed to be Kupffer cells is evident in the centrilobular region, and by Kupffer cells and intact hepatocytes at the periphery of the necrotic zones. Large numbers of neutrophils and lesser numbers of other mononuclear cells are abundant in or at the periphery of the necrotic zone (often approximating the Zone 2-3 boundary). Increased homogeneity of the hepatocytic cytoplasm with increased finely granular basophilia exists in the midzonal to ...
Bile acid synthesis defects may manifest in the neonatal period or later. This panel is specifically designed to cover the genes which lead to neonatal or infantile onset of symptoms. The Jaundice NGS Panel is an option for those cases which present with jaundice and an unclear cause.
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Accumulation of bile acids is a major mediator of cholestatic liver injury. Recent studies indicate bile acid composition between humans and rodents is dramatically different, as humans have a higher percent of glycine conjugated bile acids and increased chenodeoxycholate content, which increases the hydrophobicity index of bile acids. This increase may lead to direct toxicity that kills hepatocytes, and promotes inflammation. To address this issue, this study assessed how pathophysiological concentrations of bile acids measured in cholestatic patients affected primary human hepatocytes. Individual bile acid levels were determined in serum and bile by UPLC/QTOFMS in patients with extrahepatic cholestasis with, or without, concurrent increases in serum transaminases. Bile acid levels increased in serum of patients with liver injury, while biliary levels decreased, implicating infarction of the biliary tracts. To assess bile acid-induced toxicity in man, primary human hepatocytes were treated with ...
Bile acids are usually found conjugated to glycine or taurine, a derivative of cysteine. Cells require the presence of an active bile acid transporter for uptake of these conjugated derivatives (10). To test whether conjugated bile acids would also activate FXR, we coexpressed the human ileal bile acid transporter (IBAT) with FXR in CV-1 cells (11). FXR was strongly activated by 3 μM of the taurine or glycine conjugates of CDCA, LCA, and DCA (Fig. 2G). Weaker activation was seen with the conjugated forms of CA, and tauro-MCA was inactive (Fig. 2G). These data indicate that FXR can be activated by conjugated bile acids in tissues that express bile acid transporters such as the terminal ileum, liver, and kidney. The relation between the chemical structure of bile acids and their activation of FXR is in close agreement with the reported effects of bile acids on induction of I-BABP expression in Caco-2 cells and inhibition of Cyp7a expression in hepatocytes (3, 12). Coactivator proteins interact ...
Bile acids are steroidal amphipathic molecules derived from the catabolism of cholesterol. They modulate bile flow and lipid secretion, are essential for the absorption of dietary fats and vitamins, and have been implicated in the regulation of all the key enzymes involved in cholesterol homeostasis. Bile acids recirculate through the liver, bile ducts, small intestine and portal vein to form an enterohepatic circuit. They exist as anions at physiological pH and, consequently, require a carrier for transport across the membranes of the enterohepatic tissues. Individual bile acid carriers have now been cloned from several species. Na(+)-dependent transporters that mediate uptake into hepatocytes and reabsorption from the intestine and biliary epithelium and an ATP-dependent transporter that pumps bile acids into bile comprise the classes of transporter that are specific for bile acids. In addition, at least four human and five rat genes that code for Na(+)-independent organic anion carriers with ...
A chronic voluntary exercise paradigm, which mimics the exercise pattern of many humans, influences the hepatic clearance of several organic anions and a bile acid, whereas a neutral organic compound is seemingly unaffected. To extend these observations, the present work has evaluated in female Sprague-Dawley rats the effect of 6 weeks of voluntary running on the hepatobiliary elimination of endogenous bile acids and glutathione and exogenously injected rose bengal, digoxin, and acetaminophen. Inactive rats had mobility limited to their cages, whereas exercised rats had free access to a 44-in running wheel. In comparison to weight-matched sedentary rats, the exercised rats ran 4.3 +/- 0.3 miles/day, consumed 45% more food daily, had slightly greater liver/body weight ratios, and slightly elevated basal bile flow rates. Biliary excretion of endogenous bile acids was increased significantly, and excretion of reduced and oxidized glutathione was increased in exercised rats by 190% and 173% of ...
Obeticholic acid (OCA), a potent farnesoid X receptor agonist, was studied as monotherapy in an international, randomized, double-blind, placebo-controlled phase 2 study in patients with primary biliary cholangitis who were then followed for up to 6 years. The goals of the study were to assess the benefit of OCA in the absence of ursodeoxycholic acid, which is relevant for patients who are intolerant of ursodeoxycholic acid and at higher risk of disease progression. Patients were randomized and dosed with placebo (n = 23), OCA 10 mg (n = 20), or OCA 50 mg (n = 16) given as monotherapy once daily for 3months (1 randomized patient withdrew prior to dosing). The primary endpoint was the percent change in alkaline phosphatase from baseline to the end of the double-blind phase of the study. Secondary and exploratory endpoints included change from baseline to month 3/early termination in markers of cholestasis, hepatocellular injury, and farnesoid X receptor activation. Efficacy and safety continue to ...
Cl- secretion, the primary driving force for fluid secretion in the intestine, can become dysregulated in many pathological conditions, leading to onset of diarrhoea. However, drugs which directly target epithelial transport proteins for treatment of diarrhoeal diseases are still lacking. We have previously shown that activation of the nuclear bile acid receptor, farnesoid X receptor (FXR), potently inhibits epithelial Cl- secretion in vitro and in vivo, an effect which is mediated by a decrease in Na+-K+-ATPase activity, without altering cellular expression of the protein. Here, we sought to investigate the effects of FXR activation on the activity and expression of CFTR, the primary exit pathway for Cl- in epithelial cells. Methods: GW4064 was used as a prototypical FXR agonist. T84 cell monolayers were mounted in Ussing chambers and Cl- secretion was measured as changes in short-circuit current. Protein expression was measured by RT-PCR and western blotting. Data are presented as mean ± SEM ...
Effects of 17α-ethinylestradiol (EE) on the neutral and acidic biosynthetic pathways of bile salt (BS) synthesis were evaluated in rats with an intact enterohepatic circulation and in rats with long-term bile diversion to induce BS synthesis. For this purpose, bile salt pool composition, synthesis of individual BS in vivo, hepatic activities, and expression levels of cholesterol 7α-hydroxylase (CYP7A), and sterol 27-hydroxylase (CYP27), as well as of other enzymes involved in BS synthesis, were analyzed in rats treated with EE (5 mg/kg, 3 days) or its vehicle. BS pool size was decreased by 27% but total BS synthesis was not affected by EE in intact rats. Synthesis of cholate was reduced by 68% in EE-treated rats, while that of chenodeoxycholate was increased by 60%. The recently identified Δ,sup,22,/sup,- isomer of β-muricholate contributed for 5.4% and 18.3% (P , 0.01) to the pool in control and EE-treated rats, respectively, but could not be detected in bile after exhaustion of the pool. A ...
The effect of exercise training on upregulation of molecular markers of bile acid metabolism in the liver of ovariectomized rats fed a cholesterol-rich diet
appropriate or ideal solvent for acid due to huge solubility difference in water. The mixture constantly swirled as the mixture was being heated increases rate of dissolution and entropy of the system increasing the interaction between water and benzoic acid molecules. The complete dissolution of benzoic acid led to a clear solution. Adding the boiling chip while at room temperature. it prevents the solution from boiling over It induces boiling of the mixture, which prevents it from spilling over Activated charcoal- used for decolorization made up of finely separated C atoms w/ great surface area adsorb the impurities from solution C atoms too BIG to pass thru filter paper minimizes impurities thus increasing purity Too much charcoal may cause loss of pure substance Filter syringe used to increase purity to filter out activated charcoal & other impurities on the cotton plug Solution was filtered rapidly to have as little residue of benzoic acid crystals as possible yielded from crystallization ...
The selectivity towards CO2 during steam reforming of methanol on Pd increases in the order Al2O3 | ZrO2 | ZnO. However, conventional catalyst preparation can damage the ZnO surface, even causing complete dissolution. The faceted, prismatic ZnO crystals in the support (Aldrich) get easily destroyed during ca
A Bile acid, usually conjugated with either Glycine or Taurine. It acts as a Detergent to solubilize Fats for Intestinal Absorption and is reabsorbed by the Small Intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve Gallstones ...
The synthesis and excretion of bile acids comprise the major pathway of cholesterol catabolism in mammals. Synthesis provides a direct means of converting cholesterol, which is both hydrophobic and insoluble, into a water-soluble and readily excreted molecule, the bile acid. The biosynthetic steps t …
In this thesis, it is shown that Ero1α is expressed at a higher level in OE33 oesophageal adenocarcinoma cells than in OE21 oesophageal squamous carcinoma cells. Ero1β is not expressed in these cells. Altering pH or culture media or bile acid treatment does not cause any detectable changes in the expression or oxidation state of Ero1α, Ero1β or Protein Disulphide Isomerases (PDIs) in the OE21 and OE33 cell lines ...
The invention relates to tetrazole derivatives of bile acids, processes for their preparation, and use of these compounds as medicaments and cholesterol lowering agents. The tetrazole-bile acid derivatives are of the formula G1--X--G2, where G1 is H, a bile acid radical, or a bile acid radical which is modified on the hydroxyl functions and/or on the carboxyl group, X is a single bond or a bridge group between G1 and G2, and G2 is of the formula: ##STR1##
sodium 3alpha,7alpha-dihydroxy-12-keto-5beta-cholanate: semisynthetic bile acid with hypoglycemic efects when given orally to type 1 diabetic rats
KYBELLA™ (deoxycholic acid) injection is the first and only FDA-approved injectable treatment that is used in adults to treat the appearance and profile of moderate to severe fat below the chin (submental fat), also called, "double chin." It is not known if KYBELLA™ is safe and effective in children less than 18 years of age. It is not known if KYBELLA™ is safe and effective for use outside of submental fat. The active ingredient in KYBELLA™ is deoxycholic acid, a naturally-occurring molecule in the body that aids in the breakdown and absorption of fat. When injected into the fat beneath your chin, KYBELLA™ causes the destruction of fat cells. Once destroyed, those cells cannot store or accumulate fat ...
COUPLING METHOD FOR PEPTIDE SYNTHESIS AT ELEVATED TEMPERATURES | 3,3 DISUBSTITUTED 19-NOR PREGNANE COMPOUNDS, COMPOSITIONS, AND USES THEREOF | COMPOSITIONS AND METHODS FOR TREATING CNS DISORDERS | SYNTHETIC BILE ACID COMPOSITIONS AND METHODS | PROCESSES FOR THE PREPARATION OF ERTUGLIFLOZIN |
Tenet Diagnostics provides Bile Acids Total, Serum test with the best diagnostic center lab and well trained staff and most accurate online reports.
... / M. Ogundare; S. Theofilopoulos; A. Lockhart; L.J. Hall; E. Arenas; J. Sjövall; A.G. Brenton; Y. Wang; W.J. Griffiths ...
Kybella (deoxycholic acid) injection is the first and only FDA-approved injectable drug that contours and improves the appearance of the chin.
Subcellular localization of 3 alpha, 7 alpha-dihydroxy- and 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoyl-coenzyme A ligase(s) in rat liver ...
Systemic arterial vasodilatation has been implicated in the pathogenesis of sodium retention in cirrhosis. Hydrophobic bile acids, which have vasodilatory actions, may be involved. Ursodeoxycholic acid, a hydrophilic bile acid, could potentially decrease systemic arterial vasodilatation, possibly due to its antioxidant effects, and improve sodium handling in cirrhosis. The effects of ursodeoxycholic acid on systemic, renal and forearm haemodynamics, liver function and renal sodium handling were assessed in vasodilated cirrhotic patients with refractory ascites treated with a transjugular intrahepatic porto-systemic shunt (TIPS). Eight cirrhotic patients with refractory ascites without TIPS placement served as controls for the sodium handling effects of ursodeoxycholic acid. From 1 month post TIPS, seven patients were studied before, after 1 month of treatment with ursodeoxycholic acid (15 mg·day-1·kg-1) and at 1 month follow-up. Lipid peroxidation products were used as indices of its ...
1. Bile salt metabolism has been studied in seven patients with ileostomy following total proctocolectomy; three of these patients also had various degrees of ileal resection.. 2. The half-life of the cholic acid pool was shortened in the patients with ileal resection.. 3. Rates of bile acid synthesis were raised in two of the three patients with ileal resection. In the third, the rate was normal.. 4. Four of the six patients had low bile acid concentrations in the duodenum after a fatty meal.. 5. Deoxycholic acid could not be detected in the duodenum or ileal effluent of any of the patients.. ...
Bile acids promote bile formation and facilitate dietary lipid absorption. Animal and human studies showing disturbed bile acid metabolism in diabetes mellitus suggest a link between bile acids and glucose control. Bile acids are activating ligands of the farnesoid X receptor (FXR), a nuclear receptor with an established role in bile acid and lipid metabolism. Evidence suggests a role for FXR also in maintenance of glucose homeostasis. Animal and human studies employing bile acid sequestrants (bile acid binding agents), which interrupt the enterohepatic circulation of bile acids and effectively reduce plasma cholesterol, support a link between bile acid and glucose metabolism. In lipid-lowering trials, bile acid sequestrants, such as colesevelam hydrochloride, colestyramine (cholestyramine) and colestilan (colestimide), have also been shown to lower plasma glucose and glycosylated haemoglobin levels, suggesting the utility of these agents as a potential therapy for type 2 diabetes. In this ...
A simple, precise and sensitive method for separation and determination of total bile acid sulfates in human urine is described. The sulfate fraction of urinary bile acids was separated with lipophilic anion exchange gel, piperidinohydroxypropyl Sephadex LH-20 after sample clean-up with Sep-Pak C18 cartridge. The obtained sulfate fraction was submitted to solvolysis with a small volume of dimethoxypropane-HCl solution and subjected to enzymatic-fluorimetrical assay using 3 alpha-hydroxysteroid dehydrogenase and resazurin. In this method, no influence of existing salts in the reaction mixture on fluorescence intensity was observed and solvolysis reaction was almost complete. Overall recoveries of glycine- and taurine-conjugated bile acid 3-sulfates from normal urine ranged from 90.5 to 93.7% and those of unconjugates from 48.7 to 78.0%. The sensitivity of the described method enabled to estimate total bile acid sulfates with 0.5 ml of normal urine and precision tests showed the satisfactory accuracy. The
Cerebrotendinous xanthomatosis (CTX) is a rare, disabling genetic disorder in which cholestanol and cholesterol accumulate in the nervous system and other tissues. It has an autosomal recessive mode...
The farnesoid X receptor (FXR) regulates bile acid, lipid and glucose metabolism. Here we show that treatment of mice with glycine-b-muricholic acid (Gly-MCA) inhibits FXR signalling exclusively in intestine, and improves metabolic parameters in mouse models of obesity. Gly-MCA is a selective high-affinity FXR inhibitor that can be administered orally and prevents, or reverses, high-fat diet-induced and genetic obesity, insulin resistance and hepatic steatosis in mice. The high-affinity FXR agonist GW4064 blocks Gly-MCA action in the gut, and intestine-specific Fxr-null mice are unresponsive to the beneficial effects of Gly-MCA. Mechanistically, the metabolic improvements with Gly-MCA depend on reduced biosynthesis of intestinal-derived ceramides, which directly compromise beige fat thermogenic function. Consequently, ceramide treatment reverses the action of Gly-MCA in high-fat diet-induced obese mice. We further show that FXR signalling in ileum biopsies of humans positively correlates with ...
AIM: To determine free and conjugated serum bile acid (BA) levels in inflammatory bowel disease (IBD) subgroups with defined clinical manifestations. METHODS: Comprehensive serum BA profiling was performed in 358 IBD patients and 310 healthy controls by liquid chromatography coupled to electrospray ionization tandem mass spectrometry. RESULTS: Serum levels of hyodeoxycholic acid, the CYP3A4-mediated detoxification product of the secondary BA lithocholic acid (LCA), was increased significantly in Crohns disease (CD) and ulcerative colitis (UC), while most other serum BA species were decreased significantly. Total BA, total BA conjugate, and total BA glycoconjugate levels were decreased only in CD, whereas total unconjugated BA levels were decreased only in UC. In UC patients with hepatobiliary manifestations, the conjugated primary BAs glycocholic acid, taurocholic acid, and glycochenodeoxycholic acid were as significantly increased as the secondary BAs LCA, ursodeoxycholic acid, and ...
Peroxisomal beta-oxidation is an essential step in bile acid synthesis, since it is required for shortening of C27-bile acid intermediates to produce mature C24-bile acids. D-Bifunctional protein (DBP) is responsible for the second and third step of this beta-oxidation process. However, both patients and mice with a DBP deficiency still produce C24-bile acids, although C27-intermediates accumulate. An alternative pathway for bile acid biosynthesis involving the peroxisomal L-bifunctional protein (LBP) has been proposed. We investigated the role of LBP and DBP in bile acid synthesis by analyzing bile acids in bile, liver, and plasma from LBP, DBP, and LBP:DBP double knock-out mice. Bile acid biosynthesis, estimated by the ratio of C27/C24-bile acids, was more severely affected in double knock-out mice as compared with DBP-/- mice but was normal in LBP-/- mice. Unexpectedly, trihydroxycholestanoyl-CoA oxidase was inactive in double knock-out mice due to a peroxisomal import defect, preventing us ...
... first using chenodeoxycholic acid. He published fundamental work on the enterohepatic circulation of bile acids and how ... Thistle JL, Hofmann AF (September 1973). "Efficacy and specificity of chenodeoxycholic acid therapy for dissolving gallstones ... His early studies on the role of bile acids in the formation of micelles, the structure of the mixed micelle, and bile acid ... "Dissolution of cholesterol gallstones by chenodeoxycholic acid". N. Engl. J. Med. 286 (1): 1-8. doi:10.1056/NEJM197201062860101 ...
Hepatocytes metabolize cholesterol to cholic acid and chenodeoxycholic acid. These lipid-soluble bile acids are conjugated ( ... Finally, the conjugated bile acids which remained un-ionized conjugated bile acids are passively absorbed. Venous blood from ... Due to the pH of the small intestine, most of the bile acids are ionized and mostly occur as their sodium salts which are then ... The presence of biliary acids in the intestines helps in digestion of fats and other substances. Bilirubin is conjugated with ...
The standard treatment is chenodeoxycholic acid (CDCA) replacement therapy. Serum cholesterol levels are also followed. If ...
Chenodeoxycholic acid and other bile acids are natural ligands for FXR. Similar to other nuclear receptors, when activated, FXR ... Agonists Cafestol Chenodeoxycholic acid Obeticholic acid Fexaramine Antagonists Guggulsterone GRCh38: Ensembl release 89: ... "Farnesoid X receptor regulates bile acid-amino acid conjugation". The Journal of Biological Chemistry. 278 (30): 27703-11. doi: ... The bile acid receptor (BAR), also known as farnesoid X receptor (FXR) or NR1H4 (nuclear receptor subfamily 1, group H, member ...
The product, a combination of bezafibrate with chenodeoxycholic acid, was invented in 2001. Hepaconda is being developed as a ' ... Giaconda had initially envisaged using ursodeoxycholic acid as the bile acid in Hepaconda, but in 2006 the company shifted its ... attention to the use of chenodeoxycholic acid, having decided that its patent protection extended to all bile acid / fibrate ... combinations other than bezafibrate plus ursodoxycholic acid. Heliconda, a product for the treatment of drug-resistant ...
2006). "Transport of fluorescent chenodeoxycholic acid via the human organic anion transporters OATP1B1 and OATP1B3". J. Lipid ... 2006). "OATP8/1B3-mediated cotransport of bile acids and glutathione: an export pathway for organic anions from hepatocytes?". ... 2002). "Human organic anion transporting polypeptide 8 promoter is transactivated by the farnesoid X receptor/bile acid ... "Human organic anion transporter 1B1 and 1B3 function as bidirectional carriers and do not mediate GSH-bile acid cotransport". ...
The Australian biotech company Giaconda combines bezafibrate with chenodeoxycholic acid in an anti-hepatitis C drug combination ...
... bile acid diarrhea. The company's lead product is obeticholic acid, OCA, also known as 6-ethyl-chenodeoxycholic acid or INT-747 ... In March 2014, the company released the results of the POISE study of Obeticholic acid in PBC, which showed the drug met the ... "The Farnesoid X Receptor (FXR) Ligand Obeticholic Acid in NASH Treatment Trial(FLINT)". Archived from the original on 2014-01- ... is an American biopharmaceutical company incorporated in 2002, focusing on the development of novel synthetic bile acid analogs ...
Cholic acid Chenodeoxycholic acid Glycocholic acid Taurocholic acid Deoxycholic acid Lithocholic acid Medicine portal Animals ... such as chenodeoxycholic acid and ursodeoxycholic acid.[citation needed] On an empty stomach - after repeated vomiting, for ... As an alkali, it also has the function of neutralizing excess stomach acid before it enters the duodenum, the first section of ... A triglyceride is broken down into three fatty acids and a monoglyceride, which are absorbed by the villi on the intestine ...
MacDonald IA; Rochon YP; Hutchison DM; Holdeman LV (1982). "Formation of ursodeoxycholic acid from chenodeoxycholic acid by a 7 ...
7α-diol and then to chenodeoxycholic acid, the other major primary bile acid in humans. Serum 7α-hydroxy-4-cholesten-3-one ... The increase in serum 7α-hydroxy-4-cholesten-3-one concentrations reflects the loss of bile acids secondary to bile acid ... 12α-dihydroxycholest-4-en-3-one and then to cholic acid, the major primary bile acid in humans. Alternatively, it can be ... Elevated values are found in patients with bile acid malabsorption and may be useful in the diagnosis of this condition as high ...
... cholic acid and chenodeoxycholic acid, both of which are secreted in the bile. In the intestine these bile acids affect the ... Ellis EC (2006). "Suppression of bile acid synthesis by thyroid hormone in primary human hepatocytes". World J. Gastroenterol. ... The balance between these two steroids determines the relative amounts of the two primary bile acids, ... roles of heaptocyte nuclear factor 4alpha in mediating bile acid repression". J. Biol. Chem. 276 (45): 41690-9. doi:10.1074/jbc ...
Bacteria metabolize chenodeoxycholic acid into the secondary bile acid lithocholic acid, and they metabolize cholic acid into ... The two primary bile acids secreted by the liver are cholic acid and chenodeoxycholic acid. ... There are additional secondary bile acids, such as ursodeoxycholic acid. Deoxycholic acid is soluble in alcohol and acetic acid ... 12α-dihydroxy-5β-cholan-24-oic acid, is a bile acid. Deoxycholic acid is one of the secondary bile acids, which are metabolic ...
Muricholic acids differ from the more common bile acids, such as cholic acid or chenodeoxycholic acid, by having a hydroxyl ... α-muricholic acid β-muricholic acid γ-muricholic acid (hyocholic acid) ω-muricholic acid Russell DW (2003). "The enzymes, ... The three major bile acids in germ-free mice are cholic acid, α-muricholic, and β-muricholic acids. In conventional mice, ω- ... Muricholic acids are a group of bile acids found as one of the main forms in mice, which gives them their name, and at low ...
Cholic acid Glycocholic acid Taurocholic acid Deoxycholic acid Chenodeoxycholic acid Glycochenodeoxycholic acid ... Cholic acid is converted into deoxycholic acid and chenodeoxycholic acid into lithocholic acid. All four of these bile acids ... Bile acid synthesis occurs in liver cells which synthesize primary bile acids (cholic acid and chenodeoxycholic acid in humans ... derivatives of cholic acid) and taurochenodeoxycholic acid and glycochenodeoxycholic acid (derivatives of chenodeoxycholic acid ...
... ursodeoxycholic acid, and chenodeoxycholic acid. However, UDCA and TUDCA were first synthetically developed in 1954 in Japan. ... Tauroursodeoxycholic acid (TUDCA) is an ambiphilic bile acid. It is the taurine conjugate form of ursodeoxycholic acid (UDCA). ... Taurolithocholic acid Taurochenodeoxycholic acid, an epimer Boatright, Jeffrey H.; Nickerson, John M.; Moring, Anisha G.; ... Woo SJ, Kim JH, Yu HG (2010). "Ursodeoxycholic acid and tauroursodeoxycholic acid suppress choroidal neovascularization in a ...
Chenodeoxycholic acid-an epimer Hyodeoxycholic acid-an isomer Akare S, Jean-Louis S, Chen W, Wood DJ, Powell AA, Martinez JD ( ... While some bile acids are known to be colon tumor promoters (e.g. deoxycholic acid), others such as ursodeoxycholic acid are ... "Bile acids deoxycholic acid and ursodeoxycholic acid differentially regulate human β-defensin-1 and -2 secretion by colonic ... primary bile acids can be metabolized into secondary bile acids by intestinal bacteria. Primary and secondary bile acids help ...
... by conjugation of chenodeoxycholic acid with taurine. It is secreted into bile and then into intestine. It is usually ionized ... Taurochenodeoxycholic acid is a bile acid formed in the liver of most species, including humans, ...
... is a bile salt formed in the liver from chenodeoxycholic acid and glycine, usually found as the ... Nucleic Acids Res. 39 (Database issue): D1035-41. doi:10.1093/nar/gkq1126. PMC 3013709 . PMID 21059682. Wishart DS; Knox C; Guo ...
The natural bile acid, chenodeoxycholic acid, was identified in 1999 as the most active physiological ligand for the farnesoid ... is a semi-synthetic bile acid analogue which has the chemical structure 6α-ethyl-chenodeoxycholic acid. It is used as a drug to ... Obeticholic acid is the first FXR agonist to be used in human drug studies. Obeticholic acid is undergoing development in phase ... Bile acid diarrhea (also called bile acid malabsorption) can be secondary to Crohn's disease or be a primary condition. Reduced ...
Bacterial action in the colon produces LCA from chenodeoxycholic acid by reduction of the hydroxyl functional group at carbon-7 ... Lithocholic acid, also known as 3α-hydroxy-5β-cholan-24-oic acid or LCA, is a bile acid that acts as a detergent to solubilize ... Lithocholic acid at Sigma-Aldrich Kozoni, V.; Tsioulias, G; Shiff, S; Rigas, B (2000). "The effect of lithocholic acid on ... Dietary fiber can bind to lithocholic acid and aid in its excretion in stool; as such, fiber can protect against colon cancer. ...
... lithocholic and chenodeoxycholic acids which can form hyodeoxycholic and hyocholic acids, respectively, after 6α-hydroxilation ... "Effects of hyodeoxycholic acid and alpha-hyocholic acid, two 6 alpha-hydroxylated bile acids, on cholesterol and bile acid ... Hyodeoxycholic acid, also known as 3α,6α-Dihydroxy-5β-cholan-24-oic acid or HDCA, is a secondary bile acid, one of the ... "Formation of hyodeoxycholic acid from muricholic acid and hyocholic acid by an unidentified gram-positive rod termed HDCA-1 ...
Salts of cholic acid are called cholates. Cholic acid, along with chenodeoxycholic acid, is one of the two major bile acids ... This is why chenodeoxycholic acid, and not cholic acid, can be used to treat gallstones (because decreasing bile acid synthesis ... Cholic acid and chenodeoxycholic acid are the most important human bile acids. Other species may synthesize different bile ... Cholic acid, also known as 3α,7α,12α-trihydroxy-5β-cholan-24-oic acid is a primary bile acid that is insoluble in water ( ...
... shown to be stimulated approximately 300-fold by physiological concentrations of bile acids including chenodeoxycholic acid, ... Increases in bile acid synthesis, serum and fecal total bile acids, and specific bile acid transporters were found. Patients ... glycochenodeoxycholic acid and obeticholic acid in explants of ileal mucosa. FGF19 regulates new bile acid synthesis, acting ... In primary bile acid diarrhea, absorption of bile acids is usually normal, but defective FGF19 production can produce excessive ...
Chenodeoxycholic acid, a bile acid Deoxycholic acid, a bile acid Hyodeoxycholic acid, a bile acid Ursodiol, a bile acid. ...
A05AA01 Chenodeoxycholic acid A05AA02 Ursodeoxycholic acid A05AA03 Cholic acid A05AA04 Obeticholic acid A05AB01 Nicotinyl ... A05BA04 Citiolone A05BA05 Epomediol A05BA06 Ornithine oxoglutarate A05BA07 Tidiacic arginine A05BA08 Glycyrrhizic acid ( ...
... which is a eucaryotic receptor for bacterial surface structures such as lipoteichoic acid. ...
Chenix chenodeoxycholic acid (INN) Cheracol Cheratussin DAC CHG Scrub Chibroxin (Merck) chiniofon (INN) ChiRhoStim (ChiRhoClin ...
Cyclosporin A blocks bile acid synthesis in cultured hepatocytes by specific inhibition of chenodeoxycholic acid synthesis. H M ... Cyclosporin A blocks bile acid synthesis in cultured hepatocytes by specific inhibition of chenodeoxycholic acid synthesis ... Cyclosporin A blocks bile acid synthesis in cultured hepatocytes by specific inhibition of chenodeoxycholic acid synthesis ... Cyclosporin A blocks bile acid synthesis in cultured hepatocytes by specific inhibition of chenodeoxycholic acid synthesis ...
The glycine conjugate of CHOLIC ACID. It acts as a detergent to solubilize fats for absorption and is itself absorbed. ... Technetium Tc 99m Diethyl-iminodiacetic Acid 4. Aminopyrine (Aminophenazone) 5. Sodium 6. Chenodeoxycholic Acid (Chenix) ... Bile Acids and Salts: 3397*Cholic Acids: 8*Glycocholic Acid: 105*Glycodeoxycholic Acid: 68 ... Glycocholic Acid. Subscribe to New Research on Glycocholic Acid The glycine conjugate of CHOLIC ACID. It acts as a detergent to ...
bile acid, chenodeoxycholic acid, cholesterol, cholic acid, deoxycholic acid, hyperlipoproteinaemia, lithogenic index, ... between the proportions of deoxycholic acid and cholic acid as well as between deoxycholic acid and chenodeoxycholic acid. ... 4. Ingestion of chenodeoxycholic acid lowered serum triglyceride and deoxycholic acid lowered the serum cholesterol. ... The Formation of Deoxycholic Acid and Chenodeoxycholic Acid in Man Clin Sci Mol Med (February, 1974) ...
Chenodeoxycholic Acid (CDCA)CAS:474-25-9. Product Name: Chenodeoxycholic Acid (CDCA) Products in detail Product Name: ... Cholic acid CAS: 81-25-4. Product Name: Cholic acid Synonyms: 3,7,12-Trihydroxy-cholan-24-oic acid;5beta-Cholan-24-oic acid, ... Our main products are cholesterol, bilirubin,cholic acid, hyodeoxycholic acid, chenodeoxycholic acid, pig bile powder, ox bile ... cholic acid,ox bile powder, hyodeoxycholic acid and pig bile powder passed the certification of China GMP. ...
Berginer VM, Salen G, Sheffer S (1984) Long-term treatment of cerebrotendinous xanthomatosis with chenodeoxycholic acid. N Engl ... effect of treatment with chenodeoxycholic acid. Hepatology 7: 266-271PubMedCrossRefGoogle Scholar ... 1976) A 25-hydroxylation pathway of cholic acid biosynthesis in man and rat. J Clin Invest 57: 897-903PubMedCrossRefGoogle ... 1985) Biosynthesis of bile acids in cerebrotendinous xanthomatosis. J Clin Invest 76: 744-751PubMedCrossRefGoogle Scholar ...
Finally, we found that in ileocecal resected CD patients, the unconjugated primary BAs, cholic acid and chenodeoxycholic acid, ... Finally, we found that in ileocecal resected CD patients, the unconjugated primary BAs, cholic acid and chenodeoxycholic acid, ... taurocholic acid, and glycochenodeoxycholic acid were as significantly increased as the secondary BAs LCA, ursodeoxycholic acid ... taurocholic acid, and glycochenodeoxycholic acid were as significantly increased as the secondary BAs LCA, ursodeoxycholic acid ...
It shows great potency in treating cholestasis (bile acid backup in the liver) as the water soluble bile acids counteract the ... toxicity of regular bile acids. Can also protect and rehabilitate the liver, and general protects cells; very promising ... Competition in liver transport between chenodeoxycholic acid and ursodeoxycholic acid as a mechanism for ursodeoxycholic acid ... Tauroursodeoxycholic Acid Tauroursodeoxycholic Acid. TUDCA is a water soluble bile acid. It shows great potency in treating ...
... is a bile acid (CHEBI:3098) chenodeoxycholic acid (CHEBI:16755) is a C24-steroid (CHEBI: ... chenodeoxycholic acid (CHEBI:16755) is a dihydroxy-5β-cholanic acid (CHEBI:23775) chenodeoxycholic acid (CHEBI:16755) is ... chenodeoxycholic acid (CHEBI:16755). obeticholic acid (CHEBI:43602) has functional parent chenodeoxycholic acid (CHEBI:16755). ... chenodeoxycholic acid (CHEBI:16755) has role human metabolite (CHEBI:77746) chenodeoxycholic acid (CHEBI:16755) has role mouse ...
Advice and warnings for the use of Chenodeoxycholic acid (Chenodal) during pregnancy. FDA Pregnancy Category X - Not for use in ... Chenodeoxycholic acid Pregnancy and Breastfeeding Warnings. Chenodeoxycholic acid is also known as: Chenodal ... Chenodeoxycholic acid Breastfeeding Warnings. A decision should be made to discontinue breastfeeding or discontinue the drug, ... Chenodal (chenodeoxycholic acid)." Manchester Pharmaceutical, Fort Collins, CO. *EMEA. European Medicines Agency "EPARs. ...
Some other mammals have muricholic acid or deoxycholic acid rather than chenodeoxycholic acid. Chenodeoxycholic acid is ... Chenodeoxycholic acid (also known as chenodesoxycholic acid, chenocholic acid and 3α,7α-dihydroxy-5β-cholan-24-oic acid) is a ... Chenodeoxycholic acid has been used as medical therapy to dissolve gallstones. Chenodeoxycholic acid can be used in the ... Salts of this carboxylic acid are called chenodeoxycholates. Chenodeoxycholic acid is one of the main bile acids produced by ...
Learn about the potential side effects of chenodeoxycholic acid. Includes common and rare side effects information for ... Applies to chenodeoxycholic acid: oral tablet. Along with its needed effects, chenodeoxycholic acid may cause some unwanted ... Applies to chenodeoxycholic acid: oral tablet. Gastrointestinal. Frequency not reported: Constipation/mild intermittent ... Check with your doctor immediately if any of the following side effects occur while taking chenodeoxycholic acid:. Incidence ...
CHENODEOXYCHOLIC ACID - PHARMACOLOGY AND USE IN GALLSTONES. InPharma volume 15, pages19-20(1975)Cite this article ... CHENODEOXYCHOLIC ACID - PHARMACOLOGY AND USE IN GALLSTONES. Inpharma Wkly. 15, 19-20 (1975). https://doi.org/10.1007/BF03288109 ...
Chenodiol is made from bile acid, a substance that occurs naturally in the body. Chenodiol is used to dissolve gallstones in ... antacids that contain aluminum (such as Acid Gone, Aldroxicon, Alternagel, Di-Gel, Gaviscon, Gelusil, Maalox, Maldroxal, ... Chenodiol is made from bile acid, a substance that occurs naturally in the body. ...
... is an epimer of ursodeoxycholic acid (DB01586). Chenodeoxycholic acid is a bile acid naturally found in the body. It works by ... It can also reduce the amount of other bile acids that can be harmful to liver cells when levels are elevated. ... Chenodeoxycholic acid (or Chenodiol) is an epimer of ursodeoxycholic acid (DB01586). Chenodeoxycholic acid is a bile acid ... Receptor for bile acids such as chenodeoxycholic acid, lithocholic acid and deoxycholic acid. Represses the transcription of ...
Adjunct to bile-acid.... *Adjunct to bile-acid treatment for gall-stone dissolution: low-dose chenodeoxycholic acid combined ... Adjunct to bile-acid treatment for gall-stone dissolution: low-dose chenodeoxycholic acid combined with a terpene preparation. ... Adjunct to bile-acid treatment for gall-stone dissolution: low-dose chenodeoxycholic acid combined with a terpene preparation. ... Adjunct to bile-acid treatment for gall-stone dissolution: low-dose chenodeoxycholic acid combined with a terpene preparation. ...
Hematopoietically expressed homeobox is a target gene of farnesoid X receptor in chenodeoxycholic acid-induced liver ... Hematopoietically expressed homeobox is a target gene of farnesoid X receptor in chenodeoxycholic acid-induced liver ...
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chenodeoxycholic acid answers are found in the Tabers Medical Dictionary powered by Unbound Medicine. Available for iPhone, ... chenodeoxycholic acid is a topic covered in the Tabers Medical Dictionary. To view the entire topic, please sign in or ... "Chenodeoxycholic Acid." Tabers Medical Dictionary, 23rd ed., F.A. Davis Company, 2017. Tabers Online, www.tabers.com/ ... tabersonline/view/Tabers-Dictionary/730193/all/chenodeoxycholic_acid. Chenodeoxycholic acid. In: Venes D, ed. Tabers Medical ...
In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled ... The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity Cell Metab. 2015 Sep 1;22(3):418-26. doi: ... Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity. ... In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled ...
Tint, G. S., Salen, G., and Shefer, S.: Effect of ursodeoxycholic acid and chenodeoxycholic acid on cholesterol and bile acid ... Ursodeoxycholic acid versus chenodeoxycholic acid. Comparison of their effects on bile acid and bile lipid composition in ... Fedorowski, T., Salen, G., Tint, G. S., and Mosbach, E.: Transformation of chenodeoxycholic acid and ursodeoxycholic acid by ... Maxwell R.A., Eckhardt S.B. (1990) Chenodeoxycholic Acid and Ursodeoxycholic Acid. In: Drug Discovery. Humana Press, Totowa, NJ ...
Chenodeoxycholic acid glycine conjugate is an acyl glycine and a bile acid-glycine conugate. It is a secondary bile acid ... The major components of bile are cholic acid and chenodeoxycholic acid. In a first step the bile acids are converted to an acyl ... Thereby detoxify xenobiotics, such as benzoic acid or salicylic acid, and endogenous organic acids, such as isovaleric acid. ... In hepatocytes, both primary and secondary bile acids undergo amino acid conjugation at the C-24 carboxylic acid on the side ...
Looking for abbreviations of TCDCA? It is Tauro-Chenodeoxycholic Acid. Tauro-Chenodeoxycholic Acid listed as TCDCA ... Tauro-Chenodeoxycholic Acid - How is Tauro-Chenodeoxycholic Acid abbreviated? https://acronyms.thefreedictionary.com/Tauro- ... a href=https://acronyms.thefreedictionary.com/Tauro-Chenodeoxycholic+Acid,TCDCA,/a,. *Facebook ...
Chenodiol (Chenodeoxycholic Acid) for Dissolution of Gallstones: The National Cooperative Gallstone Study: A Controlled Trial ... Chenodiol (Chenodeoxycholic Acid) for Dissolution of Gallstones: The National Cooperative Gallstone Study: A Controlled Trial ... A double-masked study was conducted to determine the efficacy and safety of randomly allocated chenodiol (chenodeoxycholic acid ...
Combination therapy with oral ursodeoxycholic and chenodeoxycholic acids: pretreatment computed tomography of the gall bladder ... Combination therapy with oral ursodeoxycholic and chenodeoxycholic acids: pretreatment computed tomography of the gall bladder ... 55 patients with radiolucent gall stones were treated with the combination of 7.5 mg chenodeoxycholic acid (CDCA) and 5.0 mg ... Side effects were few but four patients could not tolerate the prescribed bile acids because of diarrhoea or nausea. Analysis ...
Bile acid that has been shown to increase intracellular Ca2+ in isolated rat hepatocyte couplets. Induces a permeability ... Chenodeoxycholic Acid, Sodium Salt - CAS 2646-38-0 - Calbiochem. 220411 , Chenodeoxycholic Acid, Sodium Salt - CAS 2646-38-0 - ... Bile acid that has been shown to increase intracellular Ca2+ in isolated rat hepatocyte couplets. Induces a permeability ... Bile acid that has been shown to increase intracellular Ca2+ in isolated rat hepatocyte couplets. Induces a permeability ...
  • 1. The duodenal bile acid composition was analysed in 24 control subjects and 107 patients with various types of hyperlipoproteinaemia. (portlandpress.com)
  • Our production management is strictly conducted by the requirement of GMP of China,ISO9001-2008, and all of our products could meet the requirements of international standards.In 2013, products including cholesterol, bilirubin, cholic acid,ox bile powder, hyodeoxycholic acid and pig bile powder passed the certification of China GMP. (kitairu.net)
  • Tauroursodeoxycholic acid, more commonly referred to as TUDCA, is a bile salt that is found natrually occurring in the body. (examine.com)
  • You are now following Tauroursodeoxycholic Acid. (examine.com)
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