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Taurocholic acid
Taurocholic acid
Taurocholic acid
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Taurocholic acid
Taurocholic acid
Taurocholic acid
Names
IUPAC name
2-(3α,7α,12α-Trihydroxy-5β-cholan-24-amido)ethane-1-sulfonic acid
Systematic IUPAC name
2-{(4R)-4-[(1R,3aS,3bR,4R,5aS,7R,9aS,9bS,11S,11aR)-4,7,11-Trihydroxy-9a,11a-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-1-yl]pentanamido}ethane-1-sulfonic acid
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.001.216 Edit this at Wikidata
UNII
  • InChI=1S/C26H45NO7S/c1-15(4-7-23(31)27-10-11-35(32,33)34)18-5-6-19-24-20(14-22(30)26(18,19)3)25(2)9-8-17(28)12-16(25)13-21(24)29/h15-22,24,28-30H,4-14H2,1-3H3,(H,27,31)(H,32,33,34)/t15-,16+,17-,18-,19+,20+,21-,22+,24+,25+,26-/m1/s1 checkY
    Key: WBWWGRHZICKQGZ-HZAMXZRMSA-N checkY
  • InChI=1/C26H45NO7S/c1-15(4-7-23(31)27-10-11-35(32,33)34)18-5-6-19-24-20(14-22(30)26(18,19)3)25(2)9-8-17(28)12-16(25)13-21(24)29/h15-22,24,28-30H,4-14H2,1-3H3,(H,27,31)(H,32,33,34)/t15-,16+,17-,18-,19+,20+,21-,22+,24+,25+,26-/m1/s1
    Key: WBWWGRHZICKQGZ-HZAMXZRMBW
  • C[C@H](CCC(=O)NCCS(=O)(=O)O)[C@H]1CC[C@@H]2[C@@]1([C@H](C[C@H]3[C@H]2[C@@H](C[C@H]4[C@@]3(CC[C@H](C4)O)C)O)O)C
Properties
C26H45NO7S
Molar mass 515.7058 g/mol
Melting point 125.0 °C (257.0 °F; 398.1 K)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

Taurocholic acid, known also as cholaic acid, cholyltaurine, or acidum cholatauricum, is a deliquescent yellowish crystalline bile acid involved in the emulsification of fats. It occurs as a sodium salt in the bile of mammals. It is a conjugate of cholic acid with taurine. In medical use, it is administered as a cholagogue and choleretic.[1]

Hydrolysis of taurocholic acid yields taurine.

For commercial use, taurocholic acid is manufactured from cattle bile, a byproduct of the meat-processing industry.[2]

This acid is also one of the many molecules in the body that has cholesterol as its precursor.[citation needed]

In a large prospective study (involving 569 incident colon cancer cases and 569 matched controls) it was found that prediagnostic concentrations of circulating taurocholic acid, as well as six other bile acids, were statistically significantly associated with increased colon cancer risk.[3]

Toxicity

[edit]

The median lethal dose of taurocholic acid in newborn rats is 380 mg/kg.[citation needed]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Taurocholic acid

View on Grokipedia
from Grokipedia
Taurocholic acid is a conjugate formed by the amidation of cholic acid with , serving as a key component of in mammals. It has the molecular formula C26H45NO7S and a molecular weight of 515.7 g/mol, typically occurring as a white to off-white crystalline powder that decomposes around 125 °C and exhibits good in water. Synthesized in the liver from through a series of enzymatic reactions, it is conjugated to enhance and secreted into the as the sodium salt for storage. In the , taurocholic acid plays a crucial role in lipid digestion by acting as a detergent-like that emulsifies fats and phospholipids, enabling their breakdown by lipases and subsequent absorption in the . Following its digestive function, approximately 95% of taurocholic acid is reabsorbed in the via the apical sodium-dependent transporter (ASBT) and returned to the liver through the for reuse in the , minimizing the need for . This recycling process conserves and maintains pool , with taurocholic acid representing a major conjugated form in human bile. Beyond digestion, taurocholic acid influences composition by serving as a substrate for bacterial , potentially leading to the production of secondary bile acids like , which can affect colon health. It also exhibits properties that help regulate intestinal microbial populations and has been implicated in signaling pathways, such as of the TGR5 receptor, which may contribute to metabolic regulation including glycemic control. Disruptions in taurocholic acid levels are associated with liver disorders like and , where altered conjugation and synthesis impact hepatobiliary function.

Chemical properties

Molecular structure

Taurocholic acid possesses the C26H45NO7S and a molecular weight of 515.7 g/mol. This compound arises from the conjugation of cholic acid—a trihydroxy featuring hydroxyl groups at the 3α, 7α, and 12α positions—to (2-aminoethanesulfonic acid) via an amide bond formed at the C-24 carboxyl group of cholic acid. The core stereochemical framework consists of a 5β-cholan-24-oic backbone, with the hydroxyl groups oriented in the α configuration at positions 3, 7, and 12, contributing to its specific three-dimensional arrangement essential for biological interactions. The molecular structure is depicted in SMILES notation as:

[H][C@@]1(CC[C@@]2([H])[C@]3([H])[C@H](O)C[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])C[C@H](O)[C@]12C)[C@H](C)CCC(=O)NCCS(O)(=O)=O

[H][C@@]1(CC[C@@]2([H])[C@]3([H])[C@H](O)C[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])C[C@H](O)[C@]12C)[C@H](C)CCC(=O)NCCS(O)(=O)=O

Taurocholic acid serves as a primary bile salt in mammalian bile.

Physical and chemical characteristics

Taurocholic acid is a white to off-white crystalline powder. Its melting point is approximately 125 °C, where it decomposes. Taurocholic acid exhibits high solubility in water and alcohol, attributed to its ionized sulfonate group, while it shows poor solubility in non-polar solvents. The critical micelle concentration is approximately 3-11 mM. Chemically, taurocholic acid is stable under physiological conditions, where the bond resists by pancreatic enzymes. However, it can be hydrolyzed by gut bacterial enzymes to yield cholic acid and . As an anionic , it possesses amphiphilic properties derived from its steroid-taurine conjugate structure, enabling behavior in aqueous environments. The pKa of the group is approximately 1.9, ensuring full and anionic character in at physiological . It has a specific rotation of [α]D18 +38.8° (c = 2 in alcohol).

Biosynthesis and metabolism

Biosynthesis in the liver

Taurocholic acid is synthesized in hepatocytes through the classical, or neutral, pathway of biosynthesis, which begins with the conversion of to 7α-hydroxycholesterol by the rate-limiting enzyme cholesterol 7α-hydroxylase (CYP7A1). This pathway predominates in humans and leads to the formation of cholic acid as the primary precursor for taurocholic acid. Subsequent enzymatic steps involve multiple hydroxylations and oxidations, culminating in the production of cholic acid, chemically known as 3α,7α,12α-trihydroxy-5β-cholan-24-oic acid. Cholic acid is then activated by bile acid-CoA ligase (BACL), also referred to as bile acid-CoA synthetase, which conjugates it with to form cholyl-CoA. This activation occurs at the basolateral membrane of hepatocytes, with cholyl-CoA then shuttled to peroxisomes for the subsequent conjugation step. The cholyl-CoA then reacts with in a reaction catalyzed by bile acid-CoA: N-acyltransferase (BAAT), yielding taurocholic acid. , the conjugating , is derived from metabolism in the liver via enzymes such as cysteine dioxygenase and cysteine decarboxylase. is tightly regulated by the farnesoid X receptor (FXR), which provides by inhibiting CYP7A1 transcription through induction of small heterodimer partner (SHP) and repression of key transcription factors. In humans, the daily production rate of bile acids, including precursors to taurocholic acid, ranges from 0.2 to 0.6 grams. Species differences influence conjugation patterns, with taurocholic acid being predominant in carnivores due to their high dietary availability from protein-rich diets, leading to exclusive or near-exclusive taurine amidation of s. The resulting taurocholic acid is secreted into bile canaliculi for delivery to the .

Enterohepatic circulation and microbial metabolism

Taurocholic acid, as a major conjugated , participates in the , a highly efficient process that conserves the pool in humans. Synthesized in the liver and conjugated with , it is secreted into and stored in the , with daily secretion amounting to approximately 12 to 18 grams in adults. Upon meal stimulation, is released into the , where taurocholic acid aids in emulsification before traveling through the . About 95% of s, including taurocholic acid, are reabsorbed in the via the apical sodium-dependent transporter (ASBT), facilitating active uptake into enterocytes. These reabsorbed s are then transported back to the liver via the , where they are taken up by hepatocytes through the sodium-taurocholate cotransporting polypeptide (NTCP), completing the cycle. This process repeats 6 to 10 times per day, minimizing fecal loss to roughly 0.2 to 0.6 grams daily and maintaining a total pool size of 2 to 4 grams. In the distal small intestine and colon, a portion of taurocholic acid undergoes microbial metabolism by the gut microbiota, primarily through deconjugation and subsequent modifications. Deconjugation is catalyzed by bile salt hydrolase (BSH) enzymes produced by various gut bacteria, such as species from the genera Clostridium and Bacteroides, cleaving the amide bond to yield free cholic acid and taurine. This initial step is essential for further transformations, including 7α-dehydroxylation, predominantly performed by anaerobic bacteria like Clostridium scindens, which converts cholic acid into the secondary bile acid deoxycholic acid. These microbial activities occur mainly in the colon, where about 5% of bile acids escape ileal reabsorption, and the resulting secondary bile acids can be partially reabsorbed and recirculated to the liver. The implications of this are multifaceted, influencing both host physiology and microbial ecology. Deconjugation increases the hydrophobicity and potential toxicity of s, as unconjugated forms like cholic acid are more detergent-like and can disrupt bacterial membranes, thereby shaping the composition of the . The released serves as a source, promoting the growth of taurine-utilizing and supporting overall microbial diversity. Furthermore, the high efficiency of enterohepatic reabsorption, enhanced by these processes, conserves -derived s, reducing the daily synthetic demand on the liver and preventing excessive depletion. Disruptions in this system, such as antibiotic administration that inhibits BSH activity or from dietary changes, can alter the bile acid pool composition, leading to increased conjugated s, impaired reabsorption, and clinical manifestations like or fat malabsorption.

Physiological functions

Role in digestion

Taurocholic acid, a primary taurine-conjugated , serves as a key emulsifier in the of dietary within the . Its amphiphilic structure enables the formation of mixed micelles incorporating phospholipids and at the neutral of the intestinal lumen, thereby dispersing large globules into smaller droplets and significantly increasing the surface area accessible to pancreatic s for hydrolyzing triglycerides into monoglycerides and free fatty acids. This process is essential for efficient lipid breakdown, as without adequate emulsification, lipase activity would be severely limited. By solubilizing the lipolytic products within these micelles, taurocholic acid promotes their diffusion across the unstirred water layer to the of enterocytes, where they are absorbed and reassembled into chylomicrons for transport. Furthermore, these micelles incorporate fat-soluble vitamins such as A, D, E, and K, enhancing their and preventing deficiencies that could arise from impaired absorption. Taurocholic acid constitutes approximately 10-15% of the total salt pool in humans, underscoring its prominence in these mechanisms. In human bile, taurocholic acid reaches concentrations of 10-20 mM within the , where bile is stored and concentrated; upon release in response to meals, this is diluted approximately 10-fold in the to maintain effective formation without toxicity. Due to the efficient , which reabsorbs over 95% of bile acids daily in the , the enterohepatic pool of taurocholic acid has a biological of about 4-5 days, allowing repeated use in . Deficiency in taurocholic acid or the broader bile salt pool, often from ileal dysfunction or , results in characterized by excessive fecal fat excretion and of lipids and vitamins.

Other biological roles

Taurocholic acid functions as an endogenous signaling molecule by binding to and activating the farnesoid X receptor (FXR), a that upregulates its own expression in macrophages and hepatocytes, thereby regulating glucose and as well as . It also activates the G-protein-coupled receptor TGR5, which promotes hepatic and influences in models such as mice and dairy cows. Through these receptors, taurocholic acid inhibits inflammation by suppressing signaling and modulates gut barrier integrity by promoting intestinal epithelial cell proteins like ZO-1 and . In antidiabetic mechanisms, taurocholic acid protects pancreatic β-cell viability and supports insulin secretion, exerting beneficial effects on β-cells in diabetic models while increasing concentrations in serum during development. It enhances insulin sensitivity and reduces via FXR-dependent pathways, including upregulation of fibroblast growth factor 15 (FGF15) in the , which improves oral glucose tolerance through a gut-brain axis. These effects highlight its role in maintaining glucose beyond digestive functions. Taurocholic acid demonstrates anti-inflammatory properties by reducing pro-inflammatory production, including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), in lipopolysaccharide-stimulated and models. This suppression occurs via FXR-mediated inhibition of activation, limiting recruitment and expression like CCL-2. As a primary substrate for the bile salt export pump (BSEP) and (MRP2), taurocholic acid undergoes active efflux from hepatocytes into canaliculi, supporting the vectorial transport and clearance of bile acids alongside xenobiotics to prevent intracellular accumulation. Taurocholic acid influences composition by promoting the germination of pathogenic spores in the presence of , facilitating colonization under dysbiotic conditions such as exposure. Elevated levels of taurocholic acid are negatively correlated with beneficial bacteria like , potentially hindering their infiltration and altering microbial balance in obese models.

Medical applications

Therapeutic uses

Bile acids have been employed historically since the early 1900s as bile-derived tonics and laxatives to promote digestive health, with taurocholic acid as a major conjugated form in such preparations. As a and choleretic agent, it stimulates secretion and flow, facilitating fat emulsification and absorption in the intestine. This property supports its application in managing conditions involving impaired bile production, such as , where it helps alleviate bile flow obstruction. Additionally, taurocholic acid contributes to reducing intestinal absorption and has been investigated for its role in dissolving gallstones through bile salt solutions that promote stone fragmentation and weight reduction. In preclinical models, taurocholic acid demonstrates antidiabetic potential by enhancing glycemic control, particularly as an absorption enhancer in oral insulin formulations to improve bioavailability and mitigate postprandial hyperglycemia via farnesoid X receptor (FXR) modulation. Taurocholic acid exhibits anti-inflammatory effects, notably in mouse models of trinitrobenzene sulfonic acid-induced ulcerative colitis, where it reduces colonic inflammation and tissue damage. When combined with glycocholic acid, it further inhibits pro-inflammatory cytokine production in various inflammatory contexts, supporting its low-toxicity profile for potential long-term applications in conditions like inflammatory bowel disease. For liver diseases involving conjugation defects, such as bile acid-CoA:amino acid N-acyltransferase (BAAT) deficiency, bile acid replacement therapy using glycocholic acid or cholic acid restores conjugated pools, improves fat-soluble absorption, and prevents cholestatic complications; taurocholic acid has been investigated in preclinical mouse models for similar purposes. In 2023, taurocholic acid sodium hydrate was identified in preclinical studies as a potential repurposing drug for degeneration by targeting MAPK3.

Diagnostic applications

Taurocholic acid serves as a key component in the bile acid absorption test, where radiolabeled ^{14}C-taurocholic acid is administered orally to evaluate ileal of s. In this test, patients ingest a small dose of the labeled , and fecal is measured over 48 to 72 hours; normal values indicate less than 10% , reflecting efficient , while higher levels suggest syndromes such as those associated with ileal dysfunction. Elevated serum levels of taurocholic acid act as a for and , particularly in conditions like drug-induced liver damage. In prospective studies of patients with drug-induced liver injury (DILI), taurocholic acid concentrations correlated positively with disease severity, such as bilirubin levels exceeding 20 times the upper limit of normal, with median levels reaching 10,152–28,538 nmol/L in severe cases compared to 1,955 nmol/L in milder ones. Levels above 1,955 nmol/L also predicted poor biochemical resolution at six months, with an area under the curve (AUROC) of 0.69 (sensitivity 0.81, specificity 0.57), improving to 0.81 when combined with age and severity metrics. In models of liver toxicity, serum taurocholic acid alongside cholic and glycocholic acids demonstrated superior sensitivity for detecting early cholestatic injury compared to traditional liver enzymes. In applications, taurocholic acid is quantified in plasma using liquid chromatography-mass spectrometry (LC-MS) to assess progression of liver and risks associated with colon cancer. Plasma levels of taurocholic acid are elevated in cirrhotic patients due to impaired hepatic clearance and increased , serving as a liver-specific in untargeted profiling studies that differentiate chronic , , and . Prediagnostic plasma taurocholic acid concentrations show positive associations with colon cancer risk, particularly through microbial deconjugation pathways that alter fecal metabolites, enabling risk stratification in large cohorts via targeted LC-MS panels. The use of taurocholic acid in diagnostics originated in the for evaluating syndromes, with ^{14}C-labeled versions introduced as breath and fecal tests to quantify ileal function, predating modern methods like . These early tests offered higher sensitivity for detecting subtle ileal defects compared to other acids, as taurocholic acid more closely mimics physiological conjugated forms. Despite its utility, taurocholic acid-based diagnostics face limitations, including variability influenced by dietary factors and composition, which can alter absorption and serum profiles. Radiolabeling for absorption tests is invasive and not routinely used due to and logistical demands, leading to replacement by non-radioactive alternatives in many settings.

Toxicity and safety

Acute toxicity

Taurocholic acid exhibits moderate in animal models, with the intraperitoneal LD50 reported as approximately 450 mg/kg in rats. shows lower toxicity, with an LD50 exceeding 5,000 mg/kg in rats, attributable to poor intestinal absorption and rapid biliary . Acute exposure primarily manifests as gastrointestinal irritation, including from osmotic effects in the colon, and at higher doses, due to the amphiphilic structure of taurocholic acid enabling membrane disruption akin to its properties. In , acute effects such as transient liver increases are reversible upon cessation of exposure. In s, taurocholic acid exposure is rare outside endogenous production, but overdoses from acid-containing supplements analogously cause mild symptoms like and abdominal discomfort, with no established human LD50 due to limited data.

Pathophysiological effects

In cholestatic conditions, taurocholic acid accumulates within hepatocytes due to impaired flow, leading to characterized by and . This accumulation disrupts farnesoid X receptor (FXR) signaling, a key regulator of , exacerbating through dysregulated transport and detoxification pathways. In experimental models of intrahepatic cholestasis induced by α-naphthylisothiocyanate (ANIT), taurocholic acid serves as an early and sensitive , with elevated levels preceding overt histological damage and directly promoting hepatotoxic effects. Taurocholic acid contributes to colon cancer progression through gut , where deconjugate it to cholic acid and further convert it to secondary bile acids like , alongside production of (H₂S), both of which foster tumorigenesis by activating β-catenin signaling and promoting cellular proliferation and invasiveness. Elevated serum taurocholic acid levels also correlate with the severity of liver , reflecting impaired and increased hepatic burden. In drug-induced liver injury, such as that caused by acetaminophen, taurocholic acid levels rise markedly in serum and liver tissue, amplifying via release and immune cell infiltration. However, at lower physiological doses, taurocholic acid exhibits protective effects against hepatic by modulating immune responses and inhibiting pro-inflammatory pathways, such as through TGR5 receptor activation. Imbalances in the bile acid pool, particularly with disproportionate increases in relative to other conjugates like taurochenodeoxycholic acid, contribute to cholesterol gallstone formation by altering composition and promoting . In states of elevated , such as or dysregulated gut-liver axis, taurocholic acid has been linked to neurodegeneration, where high concentrations induce synaptic loss and through neurotoxic mechanisms in the . Probiotic interventions, particularly with Bifidobacterium species expressing bile salt hydrolase, mitigate taurocholic acid toxicity by promoting its deconjugation in the gut, which reduces hepatic accumulation, , and inflammatory damage in liver and intestinal disorders. This microbial deconjugation alters profiles to favor less toxic forms, offering a potential therapeutic strategy for bile acid-related pathologies.

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