Taurochenodeoxycholic Acid
Taurodeoxycholic Acid
Glycocholic Acid
Lithocholic Acid
Chenodeoxycholic Acid
Taurocholic Acid
Bile Acids and Salts
Cytochrome P-450 Enzyme System
Microsomes, Liver
Hydroxylation
Mixed Function Oxygenases
Evidence for an anion exchange mechanism for uptake of conjugated bile acid from the rat jejunum. (1/145)
Absorption of conjugated bile acids from the small intestine is very efficient. The mechanisms of jejunal absorption are not very well understood. The aim of this study was to clarify the mechanism of absorption of conjugated bile acid at the apical membrane of jejunal epithelial cells. Brush-border membrane vesicles from intestinal epithelial cells of the rat were prepared. Absorption of two taurine-conjugated bile acids that are representative of endogenous bile acids in many variate vertebrate species were studied. In ileal, but not jejunal brush-border membrane vesicles, transport of conjugated bile acids was cis-stimulated by sodium. Transport of conjugated bile acids was trans-stimulated by bicarbonate in the jejunum. Absorption of conjugated dihydroxy-bile acids was almost twice as fast as of trihydroxy-bile acids. Coincubation with other conjugated bile acids, bromosulfophthalein, and DIDS, as well as by incubation in the cold inhibited the transport rate effectively. Absorption of conjugated bile acids in the jejunum from the rat is driven by anion exchange and is most likely an antiport transport. (+info)Polyspecific substrate uptake by the hepatic organic anion transporter Oatp1 in stably transfected CHO cells. (2/145)
The rat liver organic anion transporting polypeptide (Oatp1) has been extensively characterized mainly in the Xenopus laevis expression system as a polyspecific carrier transporting organic anions (bile salts), neutral compounds, and even organic cations. In this study, we extended this characterization using a mammalian expression system and confirm the basolateral hepatic expression of Oatp1 with a new antibody. Besides sulfobromophthalein [Michaelis-Menten constant (Km) of approximately 3 microM], taurocholate (Km of approximately 32 microM), and estradiol- 17beta-glucuronide (Km of approximately 4 microM), substrates previously shown to be transported by Oatp1 in transfected HeLa cells, we determined the kinetic parameters for cholate (Km of approximately 54 microM), glycocholate (Km of approximately 54 microM), estrone-3-sulfate (Km of approximately 11 microM), CRC-220 (Km of approximately 57 microM), ouabain (Km of approximately 3,000 microM), and ochratoxin A (Km of approximately 29 microM) in stably transfected Chinese hamster ovary (CHO) cells. In addition, three new substrates, taurochenodeoxycholate (Km of approximately 7 microM), tauroursodeoxycholate (Km of approximately 13 microM), and dehydroepiandrosterone sulfate (Km of approximately 5 microM), were also investigated. The results establish the polyspecific nature of Oatp1 in a mammalian expression system and definitely identify conjugated dihydroxy bile salts and steroid conjugates as high-affinity endogenous substrates of Oatp1. (+info)6alpha-hydroxylation of taurochenodeoxycholic acid and lithocholic acid by CYP3A4 in human liver microsomes. (3/145)
The aim of the present study was to identify the enzymes in human liver catalyzing hydroxylations of bile acids. Fourteen recombinant expressed cytochrome P450 (CYP) enzymes, human liver microsomes from different donors, and selective cytochrome P450 inhibitors were used to study the hydroxylation of taurochenodeoxycholic acid and lithocholic acid. Recombinant expressed CYP3A4 was the only enzyme that was active towards these bile acids and the enzyme catalyzed an efficient 6alpha-hydroxylation of both taurochenodeoxycholic acid and lithocholic acid. The Vmax for 6alpha-hydroxylation of taurochenodeoxycholic acid by CYP3A4 was 18.2 nmol/nmol P450/min and the apparent Km was 90 microM. Cytochrome b5 was required for maximal activity. Human liver microsomes from 10 different donors, in which different P450 marker activities had been determined, were separately incubated with taurochenodeoxycholic acid and lithocholic acid. A strong correlation was found between 6alpha-hydroxylation of taurochenodeoxycholic acid, CYP3A levels (r2=0.97) and testosterone 6beta-hydroxylation (r2=0.9). There was also a strong correlation between 6alpha-hydroxylation of lithocholic acid, CYP3A levels and testosterone 6beta-hydroxylation (r2=0.7). Troleandomycin, a selective inhibitor of CYP3A enzymes, inhibited 6alpha-hydroxylation of taurochenodeoxycholic acid almost completely at a 10 microM concentration. Other inhibitors, such as alpha-naphthoflavone, sulfaphenazole and tranylcypromine had very little or no effect on the activity. The apparent Km for 6alpha-hydroxylation of taurochenodeoxycholic by human liver microsomes was high (716 microM). This might give an explanation for the limited formation of 6alpha-hydroxylated bile acids in healthy humans. From the present results, it can be concluded that CYP3A4 is active in the 6alpha-hydroxylation of both taurochenodeoxycholic acid and lithocholic acid in human liver. (+info)The bile acid taurochenodeoxycholate activates a phosphatidylinositol 3-kinase-dependent survival signaling cascade. (4/145)
Liver injury during cholestasis reflects a balance between the effects of toxic and nontoxic bile acids. However, the critical distinction between a toxic and nontoxic bile acid remains subtle and unclear. For example, the glycine conjugate of chenodeoxycholate (GCDC) induces hepatocyte apoptosis, whereas the taurine conjugate (TCDC) does not. We hypothesized that the dissimilar cellular responses may reflect differential activation of a phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathway. In the bile acid-transporting McNtcp.24 rat hepatoma cell line, TCDC, but not GCDC, stimulated PI3K activity. Consistent with this observation, inhibition of PI3K rendered TCDC cytotoxic, and constitutive activation of PI3K rendered GCDC nontoxic. Both Akt and the atypical protein kinase C isoform zeta (PKCzeta) have been implicated in PI3K-dependent survival signaling. However, TCDC activated PKCzeta, but not Akt. Moreover, inhibition of PKCzeta converted TCDC into a cytotoxic agent, whereas overexpression of wild-type PKCzeta blocked GCDC-induced apoptosis. We also demonstrate that TCDC activated nuclear factor kappaB (NF-kappaB) in a PI3K- and PKCzeta-dependent manner. Moreover, inhibition of NF-kappaB by an IkappaB super-repressor rendered TCDC cytotoxic, suggesting that NF-kappaB is also necessary to prevent the cytotoxic effects of TCDC. Collectively, these data suggest that some hydrophobic bile acids such as TCDC activate PI3K-dependent survival pathways, which prevent their otherwise inherent toxicity. (+info)Phosphoinositide 3-kinase-dependent Ras activation by tauroursodesoxycholate in rat liver. (5/145)
Ursodesoxycholic acid, widely used for the treatment of cholestatic liver disease, causes choleretic, anti-apoptotic and immunomodulatory effects. Here the effects on choleresis of its taurine conjugate tauroursodesoxycholate (TUDC), which is present in the enterohepatic circulation, were correlated with the activation of important elements of intracellular signal transduction in cultured rat hepatocytes and perfused rat liver. TUDC induced a time- and concentration-dependent activation of the small GTP-binding protein Ras and of phosphoinositide 3-kinase (PI 3-kinase) in cultured hepatocytes. Ras activation was dependent on PI 3-kinase activity, without the involvement of protein kinase C- and genistein-sensitive tyrosine kinases. Ras activation by TUDC was followed by an activation of the mitogen-activated protein kinases extracellular-signal-regulated kinase-1 (Erk-1) and Erk-2. In perfused rat liver, PI 3-kinase inhibitors largely abolished the stimulatory effect of TUDC on taurocholate excretion, suggesting an important role for a PI 3-kinase/Ras/Erk pathway in the choleretic effect of TUDC. (+info)Differences in Ca(2+) signaling underlie age-specific effects of secretagogues on colonic Cl(-) transport. (6/145)
Taurodeoxycholic acid (TDC) stimulates Cl(-) transport in adult (AD), but not weanling (WN) and newborn (NB), rabbit colonic epithelial cells (colonocytes). The present study demonstrates that stimuli like neurotensin (NT) are also age specific and identifies the age-dependent signaling step. Bile acid actions are segment and bile acid specific. Thus although TDC and taurochenodeoxycholate stimulate Cl(-) transport in AD distal but not proximal colon, taurocholate has no effect in either segment. TDC increases intracellular Ca(2+) concentration ([Ca(2+)](i)) in AD, but not in WN and NB, colonocytes. In AD cells, TDC (5 min) action on Cl(-) transport needs intra- but not extracellular Ca(2+). NT, histamine, and bethanechol increase Cl(-) transport and [Ca(2+)](i) in AD, but not WN, distal colonocytes. However, A-23187 increased [Ca(2+)](i) and Cl(-) transport in all age groups, suggesting that Ca(2+)-sensitive Cl(-) transport is present from birth. Study of the proximal steps in Ca(2+) signaling revealed that NT, but not TDC, activates a GTP-binding protein, Galpha(q), in AD and WN cells. In addition, although WN and AD colonocytes had similar levels of phosphatidylinositol 4,5-bisphosphate, NT and TDC increased 1,4,5-inositol trisphosphate content only in AD cells. Nonresponsiveness of WN cells to Ca(2+)-dependent stimuli, therefore, is due to the absence of measurable phospholipase C activity. Thus delays in Ca(2+) signaling afford a crucial protective mechanism to meet the changing demands of the developing colon. (+info)Characterization of bile acid transport mediated by multidrug resistance associated protein 2 and bile salt export pump. (7/145)
Biliary excretion of certain bile acids is mediated by multidrug resistance associated protein 2 (Mrp2) and the bile salt export pump (Bsep). In the present study, the transport properties of several bile acids were characterized in canalicular membrane vesicles (CMVs) isolated from Sprague--Dawley (SD) rats and Eisai hyperbilirubinemic rats (EHBR) whose Mrp2 function is hereditarily defective and in membrane vesicles isolated from Sf9 cells infected with recombinant baculovirus containing cDNAs encoding Mrp2 and Bsep. ATP-dependent uptake of [(3)H]taurochenodeoxycholate sulfate (TCDC-S) (K(m)=8.8 microM) and [(3)H]taurolithocholate sulfate (TLC-S) (K(m)=1.5 microM) was observed in CMVs from SD rats, but not from EHBR. In addition, ATP-dependent uptake of [(3)H]TLC-S (K(m)=3.9 microM) and [(3)H]taurocholate (TC) (K(m)=7.5 microM) was also observed in Mrp2- and Bsep-expressing Sf9 membrane vesicles, respectively. TCDC-S and TLC-S inhibited the ATP-dependent TC uptake into CMVs from SD rats with IC(50) values of 4.6 microM and 1.2 microM, respectively. In contrast, the corresponding values for Sf9 cells expressing Bsep were 59 and 62 microM, respectively, which were similar to those determined in CMVs from EHBR (68 and 33 microM, respectively). By co-expressing Mrp2 with Bsep in Sf9 cells, IC(50) values for membrane vesicles from these cells shifted to values comparable with those in CMVs from SD rats (4.6 and 1.2 microM). Moreover, in membrane vesicles where both Mrp2 and Bsep are co-expressed, preincubation with the sulfated bile acids potentiated their inhibitory effect on Bsep-mediated TC transport. These results can be accounted for by assuming that the sulfated bile acids trans-inhibit the Bsep-mediated transport of TC. (+info)Increased production of apolipoprotein B-containing lipoproteins in the absence of hyperlipidemia in transgenic mice expressing cholesterol 7alpha-hydroxylase. (8/145)
The finding that expression of a cholesterol 7alpha-hydroxylase (CYP7A1) transgene in cultured rat hepatoma cells caused a coordinate increase in lipogenesis and secretion of apoB-containing lipoproteins led to the hypothesis that hepatic production of apoB-containing lipoproteins may be linked to the expression of CYP7A1 (Wang, S.-L., Du, E., Martin, T. D., and Davis, R. A. (1997) J. Biol. Chem. 272, 19351-19358). To examine this hypothesis in vivo, a transgene encoding CYP7A1 driven by the constitutive liver-specific enhancer of the human apoE gene was expressed in C56BL/6 mice. The expression of CYP7A1 mRNA (20-fold), protein ( approximately 10-fold), and enzyme activity (5-fold) was markedly increased in transgenic mice compared with non-transgenic littermates. The bile acid pool of CYP7A1 transgenic mice was doubled mainly due to increased hydrophobic dihydroxy bile acids. In CYP7A1 transgenic mice, livers contained approximately 3-fold more sterol response element-binding protein-2 mRNA. Hepatic expression of mRNAs encoding lipogenic enzymes (i.e. fatty-acid synthase, acetyl-CoA carboxylase, stearoyl-CoA desaturase, squalene synthase, farnesyl-pyrophosphate synthase, 3-hydroxy-3-methylglutaryl-CoA reductase, and low density lipoprotein receptor) as well as microsomal triglyceride transfer protein were elevated approximately 3-5-fold in transgenic mice. CYP7A1 transgenic mice also displayed a >2-fold increase in hepatic production and secretion of triglyceride-rich apoB-containing lipoproteins. Despite the increased hepatic secretion of apoB-containing lipoproteins in CYP7A1 mice, plasma levels of triglycerides and cholesterol were not significantly increased. These data suggest that the 5-fold increased expression of the low density lipoprotein receptor displayed by the livers of CYP7A1 transgenic mice was sufficient to compensate for the 2-fold increase production of apoB-containing lipoproteins. These findings emphasize the important homeostatic role that CYP7A1 plays in balancing the anabolic lipoprotein assembly/secretion pathway with the cholesterol catabolic bile acid synthetic pathway. (+info)Taurochenodeoxycholic acid (TCDCA) is a bile acid that is conjugated with the amino acid taurine. Bile acids are synthesized from cholesterol in the liver and released into the small intestine to aid in the digestion and absorption of fats and fat-soluble vitamins. TCDCA, along with other bile acids, is reabsorbed in the terminal ileum and transported back to the liver through the enterohepatic circulation. It plays a role in maintaining cholesterol homeostasis and has been studied for its potential therapeutic effects in various medical conditions, including gallstones, cholestatic liver diseases, and neurological disorders.
Taurodeoxycholic acid (TDCA) is a bile acid, which is a type of organic compound that is produced in the liver and essential for the digestion and absorption of fats. It is a conjugated bile acid, meaning it is formed from the combination of a deoxycholic acid with a taurine molecule.
TDCA helps to emulsify dietary fats, making them easier to absorb in the small intestine. It also plays a role in the elimination of cholesterol from the body by promoting its conversion into bile acids and excretion through the digestive system.
Abnormal levels of TDCA and other bile acids have been associated with various medical conditions, including liver disease, gallstones, and intestinal disorders. Therefore, measuring the levels of TDCA in blood or other bodily fluids can provide valuable diagnostic information for these conditions.
I'm sorry for any confusion, but "Glycocholic Acid" is not a widely recognized or established medical term. It seems there might be a misunderstanding or a typo in your request.
If you meant "Glycocholic," it's a term that refers to a substance conjugated with glycine, which is an amino acid. This process often occurs in the liver during the metabolism of certain substances, like bile acids.
"Glycocholic" could theoretically refer to a glycine conjugate of a bile acid such as cholic acid, which would make it a derivative called "Glycocholic Acid." However, I couldn't find any specific medical or scientific literature that directly refers to "Glycocholic Acid" as a known compound or concept.
If you could provide more context or clarify your question, I would be happy to help further!
Lithocholic acid (LCA) is a secondary bile acid that is produced in the liver by bacterial modification of primary bile acids, specifically chenodeoxycholic acid. It is a steroid acid that plays a role in various physiological processes such as cholesterol metabolism, drug absorption, and gut microbiota regulation. However, high levels of LCA can be toxic to the liver and have been linked to several diseases, including colon cancer and cholestatic liver diseases.
Chenodeoxycholic acid (CDCA) is a bile acid that is naturally produced in the human body. It is formed in the liver from cholesterol and is then conjugated with glycine or taurine to become a primary bile acid. CDCA is stored in the gallbladder and released into the small intestine during digestion, where it helps to emulsify fats and facilitate their absorption.
CDCA also has important regulatory functions in the body, including acting as a signaling molecule that binds to specific receptors in the liver, intestines, and other tissues. It plays a role in glucose and lipid metabolism, inflammation, and cell growth and differentiation.
In addition to its natural functions, CDCA is also used as a medication for the treatment of certain medical conditions. For example, it is used to dissolve gallstones that are composed of cholesterol, and it is also used to treat a rare genetic disorder called cerebrotendinous xanthomatosis (CTX), which is characterized by the accumulation of CDCA and other bile acids in various tissues.
It's important to note that while CDCA has therapeutic uses, it can also have adverse effects if taken in high doses or for extended periods of time. Therefore, it should only be used under the supervision of a healthcare professional.
Taurocholic acid is a bile salt, which is a type of organic compound that plays a crucial role in the digestion and absorption of fats and fat-soluble vitamins in the small intestine. It is formed in the liver by conjugation of cholic acid with taurine, an amino sulfonic acid.
Taurocholic acid has a detergent-like effect on the lipids in our food, helping to break them down into smaller molecules that can be absorbed through the intestinal wall and transported to other parts of the body for energy production or storage. It also helps to maintain the flow of bile from the liver to the gallbladder and small intestine, where it is stored until needed for digestion.
Abnormal levels of taurocholic acid in the body have been linked to various health conditions, including gallstones, liver disease, and gastrointestinal disorders. Therefore, it is important to maintain a healthy balance of bile salts, including taurocholic acid, for optimal digestive function.
Bile acids and salts are naturally occurring steroidal compounds that play a crucial role in the digestion and absorption of lipids (fats) in the body. They are produced in the liver from cholesterol and then conjugated with glycine or taurine to form bile acids, which are subsequently converted into bile salts by the addition of a sodium or potassium ion.
Bile acids and salts are stored in the gallbladder and released into the small intestine during digestion, where they help emulsify fats, allowing them to be broken down into smaller molecules that can be absorbed by the body. They also aid in the elimination of waste products from the liver and help regulate cholesterol metabolism.
Abnormalities in bile acid synthesis or transport can lead to various medical conditions, such as cholestatic liver diseases, gallstones, and diarrhea. Therefore, understanding the role of bile acids and salts in the body is essential for diagnosing and treating these disorders.
The Cytochrome P-450 (CYP450) enzyme system is a group of enzymes found primarily in the liver, but also in other organs such as the intestines, lungs, and skin. These enzymes play a crucial role in the metabolism and biotransformation of various substances, including drugs, environmental toxins, and endogenous compounds like hormones and fatty acids.
The name "Cytochrome P-450" refers to the unique property of these enzymes to bind to carbon monoxide (CO) and form a complex that absorbs light at a wavelength of 450 nm, which can be detected spectrophotometrically.
The CYP450 enzyme system is involved in Phase I metabolism of xenobiotics, where it catalyzes oxidation reactions such as hydroxylation, dealkylation, and epoxidation. These reactions introduce functional groups into the substrate molecule, which can then undergo further modifications by other enzymes during Phase II metabolism.
There are several families and subfamilies of CYP450 enzymes, each with distinct substrate specificities and functions. Some of the most important CYP450 enzymes include:
1. CYP3A4: This is the most abundant CYP450 enzyme in the human liver and is involved in the metabolism of approximately 50% of all drugs. It also metabolizes various endogenous compounds like steroids, bile acids, and vitamin D.
2. CYP2D6: This enzyme is responsible for the metabolism of many psychotropic drugs, including antidepressants, antipsychotics, and beta-blockers. It also metabolizes some endogenous compounds like dopamine and serotonin.
3. CYP2C9: This enzyme plays a significant role in the metabolism of warfarin, phenytoin, and nonsteroidal anti-inflammatory drugs (NSAIDs).
4. CYP2C19: This enzyme is involved in the metabolism of proton pump inhibitors, antidepressants, and clopidogrel.
5. CYP2E1: This enzyme metabolizes various xenobiotics like alcohol, acetaminophen, and carbon tetrachloride, as well as some endogenous compounds like fatty acids and prostaglandins.
Genetic polymorphisms in CYP450 enzymes can significantly affect drug metabolism and response, leading to interindividual variability in drug efficacy and toxicity. Understanding the role of CYP450 enzymes in drug metabolism is crucial for optimizing pharmacotherapy and minimizing adverse effects.
Microsomes, liver refers to a subcellular fraction of liver cells (hepatocytes) that are obtained during tissue homogenization and subsequent centrifugation. These microsomal fractions are rich in membranous structures known as the endoplasmic reticulum (ER), particularly the rough ER. They are involved in various important cellular processes, most notably the metabolism of xenobiotics (foreign substances) including drugs, toxins, and carcinogens.
The liver microsomes contain a variety of enzymes, such as cytochrome P450 monooxygenases, that are crucial for phase I drug metabolism. These enzymes help in the oxidation, reduction, or hydrolysis of xenobiotics, making them more water-soluble and facilitating their excretion from the body. Additionally, liver microsomes also host other enzymes involved in phase II conjugation reactions, where the metabolites from phase I are further modified by adding polar molecules like glucuronic acid, sulfate, or acetyl groups.
In summary, liver microsomes are a subcellular fraction of liver cells that play a significant role in the metabolism and detoxification of xenobiotics, contributing to the overall protection and maintenance of cellular homeostasis within the body.
Hydroxylation is a biochemical process that involves the addition of a hydroxyl group (-OH) to a molecule, typically a steroid or xenobiotic compound. This process is primarily catalyzed by enzymes called hydroxylases, which are found in various tissues throughout the body.
In the context of medicine and biochemistry, hydroxylation can have several important functions:
1. Drug metabolism: Hydroxylation is a common way that the liver metabolizes drugs and other xenobiotic compounds. By adding a hydroxyl group to a drug molecule, it becomes more polar and water-soluble, which facilitates its excretion from the body.
2. Steroid hormone biosynthesis: Hydroxylation is an essential step in the biosynthesis of many steroid hormones, including cortisol, aldosterone, and the sex hormones estrogen and testosterone. These hormones are synthesized from cholesterol through a series of enzymatic reactions that involve hydroxylation at various steps.
3. Vitamin D activation: Hydroxylation is also necessary for the activation of vitamin D in the body. In order to become biologically active, vitamin D must undergo two successive hydroxylations, first in the liver and then in the kidneys.
4. Toxin degradation: Some toxic compounds can be rendered less harmful through hydroxylation. For example, phenol, a toxic compound found in cigarette smoke and some industrial chemicals, can be converted to a less toxic form through hydroxylation by enzymes in the liver.
Overall, hydroxylation is an important biochemical process that plays a critical role in various physiological functions, including drug metabolism, hormone biosynthesis, and toxin degradation.
Mixed Function Oxygenases (MFOs) are a type of enzyme that catalyze the addition of one atom each from molecular oxygen (O2) to a substrate, while reducing the other oxygen atom to water. These enzymes play a crucial role in the metabolism of various endogenous and exogenous compounds, including drugs, carcinogens, and environmental pollutants.
MFOs are primarily located in the endoplasmic reticulum of cells and consist of two subunits: a flavoprotein component that contains FAD or FMN as a cofactor, and an iron-containing heme protein. The most well-known example of MFO is cytochrome P450, which is involved in the oxidation of xenobiotics and endogenous compounds such as steroids, fatty acids, and vitamins.
MFOs can catalyze a variety of reactions, including hydroxylation, epoxidation, dealkylation, and deamination, among others. These reactions often lead to the activation or detoxification of xenobiotics, making MFOs an important component of the body's defense system against foreign substances. However, in some cases, these reactions can also produce reactive intermediates that may cause toxicity or contribute to the development of diseases such as cancer.
Taurochenodeoxycholic acid - Wikipedia
taurochenodeoxycholic acid | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY
Serum metabolic profiling of targeted bile acids reveals potentially novel biomarkers for primary biliary cholangitis and...
Dietary Fiber | Capsaicin | Bile Acid | Gut Microbiota | Short-chain Fatty Acids
Differences in the metabolism and disposition of ursodeoxycholic acid and of its taurine-conjugated species in patients with...
WikiGenes - Hyocholic acid - 4-[(5S,8S,10R,13R,17R)-3,6,7-trihydroxy-10...
Intrahepatic Cholestasis of Pregnancy: Background, Pathophysiology, Epidemiology
Baseline metabolites could predict responders with hepatitis B virus-related liver fibrosis for entecavir or combined with...
Bile Acid Conjugates
glycine-d5 - Ontology Browser - Rat Genome Database
Environmental Chemical Contribution to the Modulation of Bile Acid Homeostasis and Farnesoid X Receptor Signaling | Drug...
Bone cell patented technology retrieval search results - Eureka | Patsnap
China good quality Refined Organic Chemicals -5000MT/Year on sales
Words in 23 letters with Y
Food Grade Tauroursodeoxycholic Acid TUDCA - Fruiterco
Bile acids and derivatives | VIOCHEMICALS
Search | Global Index Medicus
Galactosamine. Medical search. Definitions
Environmental enteric dysfunction is associated with altered bile acid metabolism<...
Publikationer - Institutionen för farmaceutisk biovetenskap - Uppsala universitet
Pesquisa | Portal Regional da BVS
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
Chapter Summary, Questions Answers - Cholesterol, Lipoprotein, and Steroid Metabolism - Biochemistry
Oleanolic acid solution (OA) is normally a triterpenoids that exists widely - PARG inhibitors in cancer therapy
Celecoxib and Tauro-Ursodeoxycholic Acid Co-Treatment Inhibits Cell Growth in Familial Adenomatous Polyposis Derived LT97 Colon...
Serum8
- Affected individuals have a defect involving the excretion of bile salts, which leads to increased serum bile acids. (medscape.com)
- Serum bile acids were measured using stable-isotope liquid chromatography-tandem mass spectrometry. (johnshopkins.edu)
- Results: In the overall study population, serum cholic acid and chenodeoxycholic acid were lower, whereas glycocholic acid, taurodeoxycholic acid, glycodeoxycholic acid, glycolithocholic acid, and glycoursodeoxycholic acid were significantly higher at older ages. (johnshopkins.edu)
- Independent of age, serum taurochenodeoxycholic acid, tauromuricholic acid, and glycoursodeoxycholic acid were significantly different between 244 children with EED and 69 children without EED. (johnshopkins.edu)
- Total serum bile acids (median, interquartile range) were 4.51 (2.45, 7.51) and 5.10 (3.32, 9.01) μmol/L in children with and without EED, respectively (age-adjusted, P=0.0009). (johnshopkins.edu)
- Fig. 1B illustrates that OA at dosages of 45 mg/kg or more elevated serum concentrations of total bile acids, with 90 mg/kg Crizotinib or more elevated total bilirubin and immediate bilirubin, all indicative of liver organ injury. (bibf1120.com)
- The bile acidity concentrations weren't further elevated with the best dosage, possibly because of saturation of serum bile acids or liver organ toxicity. (bibf1120.com)
- Twentyfour hr following the last dosage, blood was gathered and serum concentrations of bile acids and their metabolites had been dependant on UPLC-MS/MS and normalized with the inner criteria. (bibf1120.com)
Cholic4
- Administration of 0.05 g/kg capsaicin showed the highest of tauro-alpha-muricholic acid sodium salt and tauro-beta-muricholic acid sodium salt and 0.1 g/kg capsaicin resulted in the highest of lithocholic acid, cholic acid and hyodeoxycholic acid. (ijpsonline.com)
- Subsequent enzymatic reactions catalyzed by sterol 12 α -hydroxylase (CYP8B1) and sterol 27-hyroxylase (CYP27A1), respectively, yield the primary BAs, cholic acid (CA) and chenodeoxycholic acid (CDCA). (aspetjournals.org)
- Cholic acid NEW! (viochemicals.com)
- HT-29 colon cancer cells and LT97 colorectal micro-adenoma cells derived from a patient with FAP, were exposed to low dose celecoxib and UDCA alone or in combination with tauro-cholic acid (CA) and tauro-chenodeoxycholic acid (CDCA), mimicking bile of FAP patients treated with UDCA. (fapvoice.com)
Lithocholic2
- 05). Lithocholic acid concentration was consistently higher in all biological fluids during ursodeoxycholate administration. (nih.gov)
- In the intestine, bacteria can remove the glycine and taurine and can remove a hydroxyl group from the steroid nucleus, producing the secondary bile salts, deoxycholic and lithocholic acids. (pharmacy180.com)
Taurodeoxycholic3
- Tauroursodeoxycholic acid, an epimer See article about Taurodeoxycholic acid as an interferent in Perfluorooctanesulfonic acid (PFOS) mass spectrometry analysis. (wikipedia.org)
- Taurodeoxycholic acid NEW! (viochemicals.com)
- Recent studies have implemented 2 bile acids, taurocholic and taurodeoxycholic aids, as being the specific ones elevated in ICP. (medscape.com)
Taurine8
- Taurochenodeoxycholic acid is a bile acid formed in the liver of most species, including humans, by conjugation of chenodeoxycholic acid with taurine. (wikipedia.org)
- Bile acids are naturally coupled to either glycine or taurine in the liver to form bile salt conjugates. (thebileacidsexpert.com)
- It is the taurine-conjugated form of ursodeoxycholic acid (UDCA). (fruiterco.com)
- Before the bile acids leave the liver, they are conjugated to a molecule of either glycine or taurine, producing the conjugated bile salts glycocholic or taurocholic acid and glycochenodeoxycholic or taurochenodeoxycholic acid. (pharmacy180.com)
- Taurine ( / ˈ t ɔː r iː n / ), or 2-aminoethanesulfonic acid , is a non-proteinogenic amino sulfonic acid that is widely distributed in animal tissues. (cloudfront.net)
- Synthetic taurine is obtained by the ammonolysis of isethionic acid (2-hydroxyethanesulfonic acid), which in turn is obtained from the reaction of ethylene oxide with aqueous sodium bisulfite . (cloudfront.net)
- Mammalian taurine synthesis occurs in the pancreas via the cysteine sulfinic acid pathway. (cloudfront.net)
- Cysteic acid is converted to taurine by cysteine sulfinic acid decarboxylase . (cloudfront.net)
Ursodeoxycholic4
- The results showed that the addition of capsaicin further decreased the fasting blood glucose and insulin, and increased beta-muricholic acid, deoxycholic acid, chenodeoxycholic acid, and 3 beta-ursodeoxycholic acid when compared to only high fiber diet. (ijpsonline.com)
- Interestingly, these are also the bile acids significantly decreased by ursodeoxycholic acid (UCDA), which is currently the main pharmacological treatment. (medscape.com)
- Celecoxib and Tauro-Ursodeoxycholic Acid Co-Treatment Inhibits Cell Growth in Familial Adenomatous Polyposis Derived LT97 Colon Adenoma Cells. (fapvoice.com)
- We investigated the in vitro effects on cell proliferation, apoptosis, and COX-2 expression of the potential chemopreventives celecoxib and tauro-ursodeoxycholic acid (UDCA). (fapvoice.com)
Glycodeoxycholic1
- Glycodeoxycholic acid NEW! (viochemicals.com)
Enterohepatic circulation2
- Because of abnormal gut mucosa and altered gut microbiome, EED could potentially affect the metabolism and enterohepatic circulation of bile acids. (johnshopkins.edu)
- More than 95% of the bile salts are efficiently reabsorbed in the intestinal ileum by a sodium-bile salt cotransporter, returned to the blood, and carried by albumin back to the liver where they are taken up by the hepatic form of the cotransporter and reused (enterohepatic circulation, which bile acid sequestrants reduce). (pharmacy180.com)
Fatty acids6
- Plasma parameters, gut microbiota, bile acid and short-chain fatty acids were analyzed to detect the improved effects and possible mechanisms. (ijpsonline.com)
- and increased the short-chain fatty acids, especially acetic acid and butyric acid. (ijpsonline.com)
- Results from our study indicated that the addition of capsaicin have better effects to reduce the weight, insulin and fasting blood glucose, and the possibly mechanism can be due to the changes in bile acid composition, microbial abundance and shortchain fatty acids. (ijpsonline.com)
- In addition, dietary fiber can be fermented by gut microbes into Short-Chain Fatty Acids (SCFAs), which have beneficial effects on the gut barrier and can mitigate obesity by regulating the endocrine activity[ 8 ]. (ijpsonline.com)
- Apo C-II activates endothelial lipoprotein lipase (LPL), which degrades the TAG in chylomicrons to fatty acids and glycerol. (pharmacy180.com)
- The fatty acids that are released are stored (in the adipose) or used for energy (by the muscle). (pharmacy180.com)
Taurocholic1
- Taurocholic acid NEW! (viochemicals.com)
Hydrophilic bile acid2
- Because in vitro and in vivo studies suggest that the more hydrophilic bile acid tauroursodeoxycholate has greater beneficial effects than ursodeoxycholate, we have compared for the first time the absorption, metabolism, and clinical responses to these bile acids in patients with primary biliary cirrhosis (PBC). (nih.gov)
- It is a hydrophilic bile acid and a cholesterol gallstone. (fruiterco.com)
Synthesis1
- The rate-limiting step in bile acid synthesis is catalyzed by cholesterol-7-gα-hydroxylase, which is inhibited by bile acids. (pharmacy180.com)
Glycoursodeoxycholic1
- Glycoursodeoxycholic acid NEW! (viochemicals.com)
Metabolism1
- Conclusions: EED is associated with altered bile acid metabolism in young children in rural Malawi. (johnshopkins.edu)
Sulfonic2
- It is an unusual example of a naturally occurring sulfonic acid . (cloudfront.net)
- [6] The sulfonic acid has a low p K a [7] ensuring that it is fully ionized to the sulfonate at the pHs found in the intestinal tract. (cloudfront.net)
Tauroursodeoxycholic Acid1
- Tauroursodeoxycholic acid (TUDCA) is an amphiphilic bile acid. (fruiterco.com)
Amino2
- ICE Pharma are able to supply these conjugates to a host of bile acids and we are able to conjugate alternative amino acids to provide custom products as required. (thebileacidsexpert.com)
- Twenty alpha-amino acids are the subunits which are polymerized to form proteins. (lookformedical.com)
Conjugation1
- This compound has many biological roles, such as conjugation of bile acids , antioxidation , osmoregulation , membrane stabilization , and modulation of calcium signaling . (cloudfront.net)
Enzyme2
- They are capable of converting tryptophan to nicotinic acid and are used extensively in genetic and enzyme research. (lookformedical.com)
- In this pathway, cysteine is first oxidized to its sulfinic acid, catalyzed by the enzyme cysteine dioxygenase . (cloudfront.net)
Liver2
- The impact of exposures on bile acid (BA) signaling and Farnesoid X receptor-mediated gut-liver crosstalk is emerging. (aspetjournals.org)
- It can reduce the secretion of cholesterol in the liver, reduce the saturation of cholesterol in bile, promote the secretion of bile acids, increase the solubility of cholesterol in bile, dissolve cholesterol stones or prevent the formation of stones. (fruiterco.com)
Secondary bile1
- The results of metagenomic sequencing and targeted metabolome analysis together revealed that secondary bile acid (SBA) biosynthesis was significantly activated in the cows with excessive lipolysis. (biomedcentral.com)
Ursodeoxycholate1
- Sodium ursodeoxycholate is a natural bile acid isolated from bear bile. (fruiterco.com)
Sodium salt1
- Taurolithocholic acid sodium salt NEW! (viochemicals.com)
Taurolithocholic1
- The use of an integrated analysis showed that the reduction of plasma glycolithocholic acid and taurolithocholic acid could contribute to the immunosuppression of monocytes (CD14 + MON) during excessive lipolysis by decreasing the expression of GPBAR1 . (biomedcentral.com)
Glycohyodeoxycholic1
- Glycohyodeoxycholic acid NEW! (viochemicals.com)
Glycochenodeoxycholic1
- Glycochenodeoxycholic acid NEW! (viochemicals.com)
Biosynthesis1
- A nucleoside diphosphate sugar which serves as a source of glucuronic acid for polysaccharide biosynthesis. (lookformedical.com)
Cholesterol1
- Cholesterol is a hydrophobic compound, with a single hydroxyl group located at carbon 3 of the A ring, to which a fatty acid can be attached, producing an even more hydrophobic cholesteryl ester. (pharmacy180.com)
Considerable1
- In recent years, bile acids and their derivatives have received considerable interest in drug delivery research due to their versatile role in pharmaceutical formulations. (viochemicals.com)
Form1
- Cysteine sulfinic acid, in turn, is decarboxylated by sulfinoalanine decarboxylase to form hypotaurine . (cloudfront.net)
Unique1
- The availability and low cost of bile acids along with their unique advantages turn them into attractive scaffolds for the design of novel drugs and drug carrier systems. (viochemicals.com)
Provide1
- The goal of this minireview is to provide an update on the regulation of bile acid (BA) homeostasis by the nuclear receptor Farnesoid X receptor (FXR) and the effects on this regulation by exposure to environmental or therapeutic agents. (aspetjournals.org)
Quality1
- Feathery-like degeneration is certainly a well-known quality of cholestasis, as bile acids become detergents to create feathery-like morphology (Li and Crawford, 2004). (bibf1120.com)