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 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.
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.
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.
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.
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.
A major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion.
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.
Presence or formation of GALLSTONES in the BILIARY TRACT, usually in the gallbladder (CHOLECYSTOLITHIASIS) or the common bile duct (CHOLEDOCHOLITHIASIS).
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.
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.
The glycine conjugate of CHOLIC ACID. It acts as a detergent to solubilize fats for absorption and is itself absorbed.
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.
Gastrointestinal agents that stimulate the flow of bile into the duodenum (cholagogues) or stimulate the production of bile by the liver (choleretic).
CHOLESTENES with one or more double bonds and substituted by any number of keto groups.
Derivatives of the saturated steroid cholestane with methyl groups at C-18 and C-19 and an iso-octyl side chain at C-17.
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.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
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.
Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.
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.
Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.
Recycling through liver by excretion in bile, reabsorption from intestines (INTESTINAL REABSORPTION) into portal circulation, passage back into liver, and re-excretion in bile.
A cholesterol derivative found in human feces, gallstones, eggs, and other biological matter.
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.
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.
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.
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.
A microanalytical technique combining mass spectrometry and gas chromatography for the qualitative as well as quantitative determinations of compounds.
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.
Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).
A semisynthetic bile acid made from cholic acid. It is used as a cholagogue, hydrocholeretic, diuretic, and as a diagnostic aid.
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.
Excrement from the INTESTINES, containing unabsorbed solids, waste products, secretions, and BACTERIA of the DIGESTIVE SYSTEM.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Radiography of the gallbladder after ingestion of a contrast medium.
A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.
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.
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.
Drugs used for their effects on the gastrointestinal system, as to control gastric acidity, regulate gastrointestinal motility and water flow, and improve digestion.
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 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)
Cholesterol which is substituted by a hydroxy group in any position.
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.
Surgical removal of the GALLBLADDER.
Abnormal passage in any organ of the biliary tract or between biliary organs and other organs.
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.
Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.
A family of sterols commonly found in plants and plant oils. Alpha-, beta-, and gamma-isomers have been characterized.
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)
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.
Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.
Unstable isotopes of carbon that decay or disintegrate emitting radiation. C atoms with atomic weights 10, 11, and 14-16 are radioactive carbon isotopes.
The rate dynamics in chemical or physical systems.
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.
Placing of a hydroxyl group on a compound in a position where one did not exist before. (Stedman, 26th ed)
A basic science concerned with the composition, structure, and properties of matter; and the reactions that occur between substances and the associated energy exchange.
The composition, conformation, and properties of atoms and molecules, and their reaction and interaction processes.
Cholesterol present in food, especially in animal products.
Conditions with excess LIPIDS in the blood.
Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
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)
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)

Cholelithiasis is a common condition that affects millions of people worldwide. It can occur at any age but is more common in adults over 40 years old. Women are more likely to develop cholelithiasis than men, especially during pregnancy or after childbirth.

The symptoms of cholelithiasis can vary depending on the size and location of the gallstones. Some people may not experience any symptoms at all, while others may have:

* Abdominal pain, especially in the upper right side of the abdomen
* Nausea and vomiting
* Fever
* Shaking or chills
* Loss of appetite
* Yellowing of the skin and eyes (jaundice)

If left untreated, cholelithiasis can lead to complications such as inflammation of the gallbladder (cholangitis), infection of the bile ducts (biliary sepsis), or blockage of the common bile duct. These complications can be life-threatening and require immediate medical attention.

The diagnosis of cholelithiasis is usually made through a combination of imaging tests such as ultrasound, CT scan, or MRI, and blood tests to check for signs of inflammation and liver function. Treatment options for cholelithiasis include:

* Watchful waiting: If the gallstones are small and not causing any symptoms, doctors may recommend monitoring the condition without immediate treatment.
* Medications: Oral medications such as bile salts or ursodiol can dissolve small gallstones and relieve symptoms.
* Laparoscopic cholecystectomy: A minimally invasive surgical procedure to remove the gallbladder through small incisions.
* Open cholecystectomy: An open surgery to remove the gallbladder, usually performed when the gallstones are large or there are other complications.

It is important to seek medical attention if you experience any symptoms of cholelithiasis, as early diagnosis and treatment can help prevent complications and improve outcomes.

The hallmark feature of CTX is the presence of xanthomas, which are fatty deposits that accumulate in the brain and spinal cord. These deposits can cause inflammation and damage to the surrounding tissue, leading to a range of neurological symptoms.

CTX is usually diagnosed through a combination of clinical evaluation, imaging studies such as MRI or CT scans, and laboratory tests to identify the genetic mutations responsible for the condition. There is currently no cure for CTX, but treatment options may include medications to manage seizures and other symptoms, as well as surgery to remove xanthomas in some cases.

The most common form of xanthomatosis is called familial hypercholesterolemia, which is caused by a deficiency of low-density lipoprotein (LDL) receptors in the body. This results in high levels of LDL cholesterol in the blood, which can lead to the accumulation of cholesterol and other lipids in the skin, eyes, and other tissues.

Other forms of xanthomatosis include:

* Familial apo A-1 deficiency: This is a rare disorder caused by a deficiency of apolipoprotein A-1 (apoA-1), a protein that plays a critical role in the transportation of triglycerides and cholesterol in the blood.
* familial hyperlipidemia: This is a group of rare genetic disorders that are characterized by high levels of lipids in the blood, including cholesterol and triglycerides.
* Chylomicronemia: This is a rare disorder caused by a deficiency of lipoprotein lipase, an enzyme that breaks down triglycerides in the blood.

The symptoms of xanthomatosis vary depending on the specific form of the condition and the organs affected. They may include:

* Yellowish deposits (xanthomas) on the skin, particularly on the elbows, knees, and buttocks
* Deposits in the eyes (corneal arcus)
* Fatty liver disease
* High levels of cholesterol and triglycerides in the blood
* Abdominal pain
* Weight loss

Treatment for xanthomatosis typically involves managing the underlying genetic disorder, which may involve dietary changes, medication, or other therapies. In some cases, surgery may be necessary to remove affected tissue.

In summary, xanthomatosis is a group of rare genetic disorders that are characterized by deposits of lipids in the skin and other organs. The symptoms and treatment vary depending on the specific form of the condition.

There are several types of cholestasis, including:

1. Obstructive cholestasis: This occurs when there is a blockage in the bile ducts, preventing bile from flowing freely from the liver.
2. Metabolic cholestasis: This is caused by a problem with the metabolism of bile acids in the liver.
3. Inflammatory cholestasis: This occurs when there is inflammation in the liver, which can cause scarring and impair bile flow.
4. Idiopathic cholestasis: This type of cholestasis has no identifiable cause.

Treatment for cholestasis depends on the underlying cause, but may include medications to improve bile flow, dissolve gallstones, or reduce inflammation. In severe cases, a liver transplant may be necessary. Early diagnosis and treatment can help to manage symptoms and prevent complications of cholestasis.

The most common types of biliary fistulas are:

1. Bile duct-enteric fistula: This type of fistula connects the bile ducts to the small intestine.
2. Bile duct-skin fistula: This type of fistula connects the bile ducts to the skin, which can lead to a bile leak and infection.
3. Bile duct-liver fistula: This type of fistula connects the bile ducts to the liver, which can cause bleeding and infection.

Symptoms of biliary fistula may include:

* Jaundice (yellowing of the skin and whites of the eyes)
* Pale or clay-colored stools
* Dark urine
* Fatigue
* Loss of appetite
* Weight loss

Diagnosis of biliary fistula is typically made through a combination of imaging tests such as endoscopy, CT scan, and MRI. Treatment options for biliary fistula include:

1. Endoscopic therapy: This may involve the use of an endoscope to repair or close off the fistula.
2. Surgery: In some cases, surgery may be necessary to repair or remove the damaged bile ducts.
3. Stent placement: A stent may be placed in the bile ducts to help keep them open and allow for proper drainage.

It is important to seek medical attention if you experience any symptoms of biliary fistula, as it can lead to serious complications such as infection or bleeding.

There are several types of inborn errors of lipid metabolism, each with its own unique set of symptoms and characteristics. Some of the most common include:

* Familial hypercholesterolemia: A condition that causes high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to heart disease and other health problems.
* Fabry disease: A rare genetic disorder that affects the body's ability to break down certain fats, leading to a buildup of toxic substances in the body.
* Gaucher disease: Another rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.
* Lipoid cerebral degeneration: A condition that causes fatty deposits to accumulate in the brain, leading to cognitive decline and other neurological problems.
* Tangier disease: A rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.

Inborn errors of lipid metabolism can be diagnosed through a variety of tests, including blood tests and genetic analysis. Treatment options vary depending on the specific disorder and its severity, but may include dietary changes, medication, and other therapies. With proper treatment and management, many individuals with inborn errors of lipid metabolism can lead active and fulfilling lives.

There are several types of hyperlipidemia, including:

1. High cholesterol: This is the most common type of hyperlipidemia and is characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol.
2. High triglycerides: This type of hyperlipidemia is characterized by elevated levels of triglycerides in the blood. Triglycerides are a type of fat found in the blood that is used for energy.
3. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol is known as "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for excretion. Low levels of HDL cholesterol can contribute to hyperlipidemia.

Symptoms of hyperlipidemia may include xanthomas (fatty deposits on the skin), corneal arcus (a cloudy ring around the iris of the eye), and tendon xanthomas (tender lumps under the skin). However, many people with hyperlipidemia have no symptoms at all.

Hyperlipidemia can be diagnosed through a series of blood tests that measure the levels of different types of cholesterol and triglycerides in the blood. Treatment for hyperlipidemia typically involves dietary changes, such as reducing intake of saturated fats and cholesterol, and increasing physical activity. Medications such as statins, fibric acid derivatives, and bile acid sequestrants may also be prescribed to lower cholesterol levels.

In severe cases of hyperlipidemia, atherosclerosis (hardening of the arteries) can occur, which can lead to cardiovascular disease, including heart attacks and strokes. Therefore, it is important to diagnose and treat hyperlipidemia early on to prevent these complications.

... is a primary bile acid, synthesized in the liver and present in high concentrations in bile that is used therapeutically to ... Chenodeoxycholic acid (chenodiol) is a primary bile acid, synthesized in the liver and present in high concentrations in bile ... Chenodiol (Chenodeoxycholic Acid) No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver ... Chenodiol (chenodeoxycholic acid) for dissolution of gallstones: the National Cooperative Gallstone Study. A controlled trial ...
... is a primary bile acid, synthesized in the liver and present in high concentrations in bile that is used therapeutically to ... Chenodeoxycholic acid (chenodiol) is a primary bile acid, synthesized in the liver and present in high concentrations in bile ... Chenodiol (Chenodeoxycholic Acid) No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver ... Chenodiol (chenodeoxycholic acid) for dissolution of gallstones: the National Cooperative Gallstone Study. A controlled trial ...
Bile acid receptor. Receptor for bile acids such as chenodeoxycholic acid, lithocholic acid and deoxycholic acid. Represses the ... Chenodeoxycholic acid (JP15); Anthropodesoxycholic acid; Chenodiol (USAN); 3-alpha,7-alpha-Dihydroxy-5-beta-cholan-24-oic acid ... Cholan-24-oic acid, 3,7-dihydroxy-, (3alpha,5beta,7alpha)-; CCRIS 2195; Chenodesoxycholic acid; Chenodeoxycholic acid; ... Bile acids may also bind the the bile acid receptor (FXR) which regulates the synthesis and transport of bile acids. show less ...
Chenodeoxycholic acid 750 mg. To relieve a gall bladder attack. Have on hand Heptachlor (a German herbal preparation) and take ... Most important is to have your stomach acid tested and to supplement with HCl if it is found to be low.. Vitamin C: 1 g per day ... Supplements of the amino acid tausine help to prevent gallstones (JPENS Parenter Enteral Nutr, 1991; 15: 294-7).. One of these ...
... gallstones chenodeoxycholic acids (CDCA); Ursodeoxycholic acid (UDCA, ursodiol); Endoscopic retrograde cholangiopancreatography ...
... is the non-proprietary name for chenodeoxycholic acid, a naturally occurring human bile acid. It is a bitter-tasting ... Bile acids, including Chenodiol and lithocholic acid, have no carcinogenic potential in animal models, but have been shown to ... deoxycholic acid in an expanded bile acid pool. These actions contribute to biliary cholesterol desaturation and gradual ... Bile acid sequestering agents, such as cholestyramine and colestipol, may interfere with the action of Chenodiol by reducing ...
Obeticholic acid, 6α-ethyl-chenodeoxycholic acid, is a semi-synthetic bile acid with greater activity as an FXR agonist.. ... Four times daily dosing (r.i.d.) of your proton-pump inhibitor (Insurance) attains potent acid solution hang-up, suggesting ... General, the information recommend oxidative damage to nucleic acid and a compensatory boost in OGG1 phrase occur at the ... propanoic acid solution, as a powerful and also by mouth obtainable GPR40 agonist. Compound Tough luck (DS-1558) is discovered ...
... chenodeoxycholic and deoxycholic acids are more cytotoxic than cholic acid (3). The minimum 15-mL dose of sheep bile contains ... chenodeoxycholic, 23% cholic, and 5% lithocholic acids) -- the equivalent of 36% of the maximum daily dose of bile acids used ... Chenodiol (chenodeoxycholic acid) for dissolution of gallstones: the National Cooperative Gallstone Study. Ann Intern Med 1981; ... Bobowiec R. Effects of the intravenous infusion of sodium salts of bile acids on bile flow and bile acids of sheep {Polish}. ...
Chenodeoxycholic acid. *. Closely Matching Concepts from Other Schemes. *. Cálculos biliares *. Calculs biliaires ...
7. Chenodeoxycholic acid and diarrhoea.. Corazziari E; Pozzessere C; Dani S; Piccinni-Leopardi M; Anzini F; Alessandrini A. ... 8. Chenodeoxycholic acid therapy of gallstones.. Dowling RH. Clin Gastroenterol; 1977 Jan; 6(1):141-63. PubMed ID: 330046. [No ... 1. Cyclic AMP and cyclic GMP levels in human colonic mucosa before and during chenodeoxycholic acid therapy.. Corazza GR; ... Treatment of patients with gallstones with chenodeoxycholic acid (authors transl)].. Leuschner U; Reber E; Erb W. Dtsch Med ...
Title: Differential disposition of chenodeoxycholic acid versus taurocholic acid in response to acute troglitazone exposure in ... The effects of TRO on the disposition of [(14)C]-labeled chenodeoxycholic acid ([(14)C]CDCA), an unconjugated cytotoxic BA, ... Chenodeoxycholic Acid/metabolism*; Chromans/toxicity*; Chromatography, High Pressure Liquid; Drug-Induced Liver Injury/etiology ... Typically, studies use taurocholic acid (TCA) as a model substrate to investigate effects of xenobiotics on BA disposition. ...
fats (bile acids), specifically a bile acid called chenodeoxycholic acid.Mutations in the CYP27A1 gene lead to the ... abnormal ... down cholesterol to form a bile acid called chenodeoxycholic acid. The formation of bile acids from cholesterol is ... protein ... called cholesterol to form a bile acid called chenodeoxycholic acid. Bile acids are a component of a digestive ... ... It is treated with chenodeoxycholic acid (CDCA) replacement therapy. NIH: National Institute of Neurological ... ...
Gerolami A, Sarles H. Letter: Beta-sitosterol and chenodeoxycholic acid in the treatment of cholesterol gallstones. Lancet 1975 ... Begemann, F., Bandomer, G., and Herget, H. J. The influence of beta-sitosterol on biliary cholesterol saturation and bile acid ... Part 5. Faecal short-chain fatty acid and microflora content, faecal bacterial enzyme activity and serum female sex hormones in ... Effect of beta-sitosterol alone or in combination with chenic acid on cholesterol saturation of bile and cholesterol absorption ...
With an early accurate diagnosis, CTX can be effectively treated with chenodeoxycholic acid (CDCA) replacement therapy. CDCA ... In ARD, phytanic acid accumulates and is toxic to myelin.. *Infantile Refsum disease (IRD)-an inherited disorder that damages ... People with ARD lack the enzyme in peroxisomes that breaks down phytanic acid, a type of fat found in certain foods. ... the brain chemical N-acetyl-L-aspartate or N-acetyl-L-aspartic acid. ...
Impact of dietary chenodeoxycholic acid on the hypothalamic-pituitary-adrenal axis in rats. McNeilly A , Walker B , Andrew R ... Recently we and others have demonstrated that bile acids act as potent inhibitors of GC metabolism by 5beta-reductase and ...
Vitamin D Receptor Deletion Changes Bile Acid Composition in Mice Orally Administered Chenodeoxycholic Acid.. *S. Nishida, ... Lithocholic Acid Is a Vitamin D Receptor Ligand That Acts Preferentially in the Ileum. *Michiyasu Ishizawa, D. Akagi, M. ... Results indicate that VDR deletion influences CDCA metabolism, and VDR may play a role in the excretion of excess bile acids.. ... Vitamin D3 Modulates the Expression of Bile Acid Regulatory Genes and Represses Inflammation in Bile Duct-Ligated Mice. *M. ...
A) 5α-cyprinol sulfate (5α-CPS), (B) taurochenodeoxycholic acid (TCDCA), and. (C) chenodeoxycholic acid (CDCA) on behavioral ... chenodeoxycholic acid (CAS: 474-25-9) and glycocholic acid hydrate (CAS:1192657-83-2) were of ,95% purity and obtained from ... Response of Daphnia to chenodeoxycholic acid (CDCA).. Statistical analysis of mean daytime residence depth of Daphnia magna in ... release fatty acids bound to a particular amino acid, which lead to changes in morphology in Daphnia pulex (Weiss et al., 2018 ...
UGT1A3 catalysed chenodeoxycholic acid 24-acylglucuronidation was strongly competitively inhibited by AM-2201, MAM-2201, and ...
Abstract: A multi-step synthesis of chenodeoxycholic acid from 3-keto-bisnorcholenol, a compound readily obtained from the ... Process and intermediates for the synthesis of Vitamin D.sub.3 metabolites and chenodeoxycholic acid ... and amino acid analyses of acid and enzymic hydrolysates. Bioassay of the synthetic analogs for analgesic activity by the tail- ... Abstract: Propionic acid esters of the general formula ##STR1## wherein R.sub.1 is hydrogen, alkyl of from 1 to 6 carbon atoms ...
... bile acids). Specifically, sterol 27-hydroxylase breaks down cholesterol to form a bile acid called chenodeoxycholic acid. The ... The most common mutation changes the amino acid arginine to the amino acid cysteine at position 362 in the protein (written as ... in amino acids typically disrupt the normal function of the protein and impair its ability to help form chenodeoxycholic acid. ... Norlin M, von Bahr S, Bjorkhem I, Wikvall K. On the substrate specificity of human CYP27A1: implications for bile acid and ...
... bile acids are increasingly being recognized as signaling molecules that activate cell-signaling receptors. ... In humans, the other major bile acid is chenodeoxycholic acid (CDCA). Because CDCA is converted into muricholic acid (MCA) in ... The metabolism of chenodeoxycholic acid to beta-muricholic acid in rat liver ... Cyp8b1−/− mice have an altered circulating bile acid pool. A: Plasma bile acid pool in control (+/+) and Cyp8b1−/− (−/−) mice ( ...
Deoxycholic Acid [D04.210.500.105.225.272] * Chenodeoxycholic Acid [D04.210.500.] * Glycochenodeoxycholic Acid [ ... Deoxycholic Acid [D04.210.500.221.430.342] * Chenodeoxycholic Acid [D04.210.500.221.430.342.300] * Glycochenodeoxycholic Acid [ ... Chenic Acid Chenique Acid Chenix Chenodeoxycholate Chenodiol Chenofalk Chenophalk Gallodesoxycholic Acid Henohol Quenobilan ... Chenodeoxycholic Acid Preferred Term Term UI T007659. Date01/01/1999. LexicalTag NON. ThesaurusID ...
"chenodeoxycholic acid"[MeSH Terms] OR ("chenodeoxycholic"[All Fields] AND "acid"[All Fields]) OR "chenodeoxycholic acid"[All ...
Earlier this year, Schrauwen showed that giving women a pill containing the bile acid chenodeoxycholic acid for two days did ... For instance, through the binding of a receptor called TGR5, bile acids induce brown fat cells to burn calories. ...
CAS number: 1355149-45-9 free acid Synonyms: Remdesivir metabolite. Details Chenodeoxycholic acid. Product Number: C8908 ...
CA, cholic acid; DCA, deoxycholic acid; LCA, lithocholic acid; CDCA, chenodeoxycholic acid; UDCA, ursodeoxycholic acid, ... CDCA, chenodeoxycholic acid; HDCA, hyodeoxycholic acid; HCA, hyocholic acid; CA, cholic acid; DCA, deoxycholic acid; LCA, ... Ursodeoxycholic acid, 7-ketolithocholic acid, and chenodeoxycholic acid are primary bile acids of the nutria (Myocastor coypus ... Stereocontrolled convertsion of hyodeoxycholic acid into chenodeoxycholic acid and ursodeoxycholic acid. J Chem Soc Perkin ...
Description: Our Chenodeoxycholic Acid ELISA Kit is designed for detection and quantitation of chenodeoxycholic acid in plasma ... Chenodeoxycholic acid levels in unknown samples are calculated based on a chenodeoxycholic acid standard curve. ... Orotic Acid Elisa. Lab Reagents Acid Elisa Laboratories manufactures the orotic acid elisa reagents distributed by Genprice. ... An anti-chenodeoxycholic acid antibody is added, which is then detected by an HRP conjugated secondary antibody. ...
Chenodeoxycholic Acid D4.808. D4.210.500. D4.808.221.430.342.300 D4.210.500.221.430.342.300 Child ... Amino Acid Transport System y+ D12.776.157.530.937.375 D12.776.543.585.937.375 Amino Acid Transport System y+L D12.776.157.530. ... Amino Acid Motifs G2.111.570.60.40 G2.111.570.820.709.275.500 G2.111.570.820.709.600.40 G2.111.570.820.709.600.500 Amino Acid ... Acid Rain G16.500.240.135.859.50 G16.500.175.859.50 Acid Sensing Ion Channels D12.776.543.550.425.875.50 D12.776.543.550. ...

No FAQ available that match "chenodeoxycholic acid"

No images available that match "chenodeoxycholic acid"