TLCA

TLCA
Name	TLCA
Caption	Structural formula of TLCA
Chemical formula	C?H?O?S? (unknown)

TLCA

TLCA is a bile acid derivative prominent in studies of hepatology, pharmacology, and microbial metabolism. It appears in discussions of cholestasis, nuclear receptor signaling, and enterohepatic circulation, and features in research tied to Hepatology, Gastroenterology, Pharmacology, Microbiology, and Biochemistry. Investigations of TLCA intersect with work on Farnesoid X receptor, TGR5, Primary biliary cholangitis, Cholestasis, and Bile acid sequestrants.

Definition and nomenclature

TLCA denotes a taurine-conjugated lithocholic acid, named according to bile acid conjugation conventions used in Biochemistry and Clinical chemistry. The term follows patterns established for conjugates such as taurocholic acid and taurochenodeoxycholic acid, paralleling names employed in literature from groups at National Institutes of Health, Mayo Clinic, King's College London, Harvard Medical School, and University of California, San Diego. Nomenclatural treatment aligns with IUPAC-informed systematic names applied by researchers at American Chemical Society journals and in databases curated by PubChem, ChemSpider, and Human Metabolome Database.

Chemical structure and properties

The molecule comprises a steroidal bile acid backbone derived from lithocholic acid linked to a taurine moiety, following conjugation chemistry similar to that described in reports by Royal Society of Chemistry and Journal of Biological Chemistry. Its sterane core and hydroxylation pattern influence hydrophobicity, pKa, and micelle-forming behavior examined in studies from Max Planck Society and ETH Zurich. Physical properties—solubility, partition coefficient, and critical micelle concentration—are compared in comparative analyses alongside Cholic acid, Chenodeoxycholic acid, Deoxycholic acid, and conjugates such as taurocholic acid. Structural characterization methods cited in work from Massachusetts Institute of Technology and California Institute of Technology include nuclear magnetic resonance used by groups at University of Oxford and X-ray crystallography protocols developed at Stanford University.

Biosynthesis and metabolism

TLCA is formed by hepatic conjugation of lithocholic acid with taurine via enzymatic pathways similar to those characterized by investigators at National Institute of Diabetes and Digestive and Kidney Diseases, University of Pennsylvania, and Imperial College London. This conjugation involves ligases and transferases analogous to Bile acid-CoA:amino acid N-acyltransferase activities profiled in studies from University of Cambridge and Centre National de la Recherche Scientifique. Enterohepatic circulation routes described in literature from Johns Hopkins University and University of Toronto show microbial deconjugation by gut bacteria explored by teams at Broad Institute, Wellcome Sanger Institute, and Wageningen University. Microbial genera implicated in deconjugation and 7α-dehydroxylation include species discussed in reports from Max Planck Institute for Infection Biology and University of California, Davis microbiome centers, linking TLCA dynamics to research at European Molecular Biology Laboratory and Karolinska Institute.

Biological roles and clinical significance

TLCA interacts with host receptors such as TGR5 and modulates signaling pathways including those involving Farnesoid X receptor and Pregnane X receptor, topics pursued at Scripps Research Institute, Columbia University, and Yale University. Effects on cholangiocyte physiology and hepatocyte function relate to conditions studied by clinicians at Cleveland Clinic, Mayo Clinic, and Mount Sinai Health System, notably Primary sclerosing cholangitis, Primary biliary cholangitis, and drug-induced Cholestasis. Experimental evidence from laboratories at University College London, University of Michigan, and University of California, San Francisco links TLCA to modulation of inflammatory cascades investigated in collaboration with researchers at Karolinska Institute and Institut Pasteur. TLCA concentrations are considered in toxicology assessments by agencies including Food and Drug Administration and European Medicines Agency when evaluating bile acid–related adverse effects; clinical assays are used in settings described by Mayo Clinic Laboratories and Quest Diagnostics.

Analytical methods and detection

Measurement of TLCA in biological matrices employs mass spectrometry platforms developed by groups at Thermo Fisher Scientific, Agilent Technologies, and Waters Corporation with liquid chromatography tandem mass spectrometry workflows standardized in consortia involving NIH Common Fund programs. Sample preparation methods trace to protocols from Cold Spring Harbor Laboratory and Roche Diagnostics, with derivatization and negative-ion electrospray strategies reported in Analytical Chemistry and Clinical Chemistry. Quantitation is performed alongside panels including Cholic acid, Deoxycholic acid, Chenodeoxycholic acid, tauro- and glyco-conjugates in clinical metabolomics studies from European Bioinformatics Institute, Metabolomics Society, and multicenter studies coordinated by Human Microbiome Project investigators.

History and discovery

The identification of lithocholic acid conjugates emerged from mid-20th-century bile acid chemistry carried out at institutions such as University of Göttingen, University of Edinburgh, and Karolinska Institute. Early analytical separations reported in journals associated with Royal Society of Chemistry and researchers at University of Basel set the stage for later mass spectrometric and enzymological elucidation undertaken by laboratories at NIH, University of Tokyo, and Peking University. Subsequent clinical and mechanistic interest grew through collaborations linking Harvard Medical School, Stanford Medicine, and European centers including Institut Pasteur and Max Planck Society.

Category:Bile acids