chenodeoxycholic acid

Chenodeoxycholic acid (CDCA) is 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.

Chenodeoxycholic acid 3-sulfate disodium, a bile acid, closely corresponds with the extent of hepatic dysfunction [1].

Chenodeoxycholic acid 3-sulfate, a bile acid, closely corresponds with the extent of hepatic dysfunction [1].

Glycochenodeoxycholic Acid (Lithocholylglycine) is a glycine conjugate of lithocholic acid, a bile acid. It is increased in livers of mice that are fed diets supplemented with ursadeoxycholic acid. Glycolithocholic acid levels are decreased in lean mice treated with obestatin. Serum glycolithocholic acid levels increase with age in children.

Taurochenodeoxycholic acid sodium (Sodium taurochenodeoxycholate) is one of the main bioactive substances of animals' bile acid. Taurochenodeoxycholic acid sodium induces apoptosis and shows obvious anti-inflammatory and immune regulation properties. It can increase glucose-induced insulin secretion and stimulate the electrical activity of α2-cells and enhance cytosolic Ca(2+) concentration ([Ca(2+)](c)).

Taurochenodeoxycholic Acid (12-Deoxycholyltaurine) is one of the main bioactive substances of animals' bile acid.

12-Ketochenodeoxycholic acid is a direct precursor of cholodeoxycholic acid (CDCA), which is used to treat cholesterol gallstones and possesses chemotherapeutic properties for dissolving gallstones [1].

Glycochenodeoxycholic acid sodium salt is a bile salt formed in the liver from deoxycholic acid and glycine that induces apoptosis in hepatocytes. It acts as a detergent, dissolves fats for absorption, and is itself absorbed.

Glycochenodeoxycholic acid 3-glucuronide, a steroid glucuronide and plasma metabolite, can be utilized as a biomarker in diabetes and hepatocellular carcinoma (HCC) research [1].

Bile acids are essential for solubilization and transport of dietary lipids, are the major products of cholesterol catabolism, and are physiological ligands for farnesoid X receptor (FXR), a nuclear receptor that regulates genes involved in lipid metabolism.1They are also inherently cytotoxic, as physiological imbalance contributes to increased oxidative stress.2,3Bile acid-controlled signaling pathways are promising novel targets to treat such metabolic diseases as obesity, type II diabetes, hyperlipidemia, and atherosclerosis.Guggulsterone, derived from resin of the guggul tree, is a competitive antagonist of FXR bothin vitroandin vivo.4Thecisstereoisomer of guggulsterone, (E)-guggulsterone, decreases chenodeoxycholic acid (CDCA)-induced FXR activation with an IC50value of 15 μM.5,6By inhibiting CDCA-induced transactivation of FXR, guggulsterone lowers low-density lipoprotein cholesterol and triglyceride levels in rodents fed a high cholesterol diet.4 1.Makishima, M., Okamoto, A.Y., Repa, J.J., et al.Identification of a nuclear receptor for bile acidsScience2841362-1365(1999) 2.Barbier, O., Torra, I.P., Sirvent, A., et al.FXR induces the UGT2B4 enzyme in hepatocytes: A potential mechanism of negative feedback control of FXR activityGastroenterology1241926-1940(2003) 3.Tan, K.P., Yang, M., and Ito, S.Activation of nuclear factor (erythroid-2 like) factor 2 by toxic bile acids provokes adaptive defense responses to enhance cell survival at the emergence of oxidative stressMol. Pharmacol.72(5)1380-1390(2007) 4.Urizar, N.L., Liverman, A.B., Dodds, D.T., et al.A natural product that lowers cholesterol as an anatagonist ligand for FXRScience296(5573)1703-1706(2002) 5.Cui, J., Huang, L., Zhao, A., et al.Guggulsterone is a farnesoid X receptor antagonist in coactivator association assays but acts to enhance transcription of bile salt export pumpThe Journal of Biological Chemisty278(12)10214-10220(2003) 6.Wu, J., Xia, C., Meier, J., et al.The hypolipidemic natural product guggulsterone acts as an antagonist of the bile acid receptorMolecular Endocrinology16(7)1590-1597(2002)

3α,7α-Dihydroxycoprostanic acid, an endogenous metabolite and bile acid, serves as the precursor to chenodeoxycholic acid [1].