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Discover high-quality research tools to investigate GLP-1 mechanisms and next-generation metabolic targets.
OBESITY RESEARCH SOLUTIONSCholic acid is a primary bile acid.1 It is formed from cholesterol via a multistep process catalyzed by the cytochrome P450 (CYP) isoforms CYP7A1, CYP8B1, and CYP27A1. Cholic acid is conjugated to glycine or taurine by bile acid-CoA:amino acid N-acyltransferase (BAAT) to produce glycocholic acid (GCA; Item No. 20276) and taurocholic acid (TCA; Item No. 16215), respectively, in the liver, and is transformed into the secondary bile acid deoxycholic acid (DCA; Item Nos. 20756 | 18231) by intestinal microbiota.1,2,3 It induces C. difficile colony formation in an agar dilution assay when used at a concentration of 0.1% w/v.4 Dietary administration of cholic acid (0.4% w/w) increases serum cholesterol levels, biliary phospholipid secretion, and fecal DCA levels in rats.5
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1. Bile acid synthesis: From nature to the chemical modification and synthesis and their applications as drugs and nutrients. Front. Pharmacol. 9, 939 (2018).
2. The emerging role of acyl-
3. Interaction of gut microbiota with bile acid metabolism and its influence on disease states. Appl. Microbiol. Biotechnol. 101(1), 47-64 (2017).
4. Bile salts and glycine as cogerminants for Clostridium difficile spores. J. Bacteriol. 190(7), 2505-2512 (2008).
5. Effects of cholic acid, chenodeoxycholic acid, and their related bile acids on cholesterol, phospholipid, and bile acid levels in serum, liver, bile, and feces of rats. J. Biochem. 87(1), 187-194 (1980).