Cholic acid
Cholic acid is a major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion. It prevents hepatic TG accumulation, VLDL secretion, and elevated serum TG in mouse models of hypertriglyceridemia;at the molecular level, CA decreases hepatic expression of SREBP-1c and its lipogenic target genes.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Chem Commun (Camb). 2015 Apr 20.
Design of β-CD-surfactant complex-coated liquid crystal droplets for the detection of cholic acid via competitive host-guest recognition.[Pubmed:
25892566]
β-CD-C14TAB complex-coated 5CB droplets are designed by the adsorption of β-CD-C14TAB complexes at the 5CB/aqueous interface. We show that the 5CB droplets can be used as an optical probe for the selective detection of Cholic acid in aqueous solution containing uric acid and urea via competitive host-guest recognition.
PLoS One. 2015 Feb 13;10(2):e0117599.
Cholic acid induces a Cftr dependent biliary secretion and liver growth response in mice.[Pubmed:
25680200]
The cause of Cystic fibrosis liver disease (CFLD), is unknown. It is well recognized that hepatic exposure to hydrophobic bile salts is associated with the development of liver disease. For this reason, we hypothesize that, CFTR dependent variations, in the hepatic handling of hydrophobic bile salts, are related to the development CFLD.
METHODS AND RESULTS:
To test our hypothesis we studied, in Cftr-/- and control mice, bile production, bile composition and liver pathology, in normal feeding condition and during cholate exposure, either acute (intravenous) or Cholic acid (three weeks via the diet). In Cftr-/- and control mice the basal bile production was comparable. Intravenous taurocholate increased bile production to the same extent in Cftr-/- and control mice. However, Cholic acid cholate exposure increased the bile flow significantly less in Cftr-/- mice than in controls, together with significantly higher biliary bile salt concentration in Cftr-/- mice. Prolonged cholate exposure, however, did not induce CFLD like pathology in Cftr-/- mice. Cholic acid cholate exposure did induce a significant increase in liver mass in controls that was absent in Cftr-/- mice. Cholic acid cholate administration induces a cystic fibrosis-specific hepatobiliary phenotype, including changes in bile composition. These changes could not be associated with CFLD like pathological changes in CF mouse livers. However, Cholic acid cholate administration induces liver growth in controls that is absent in Cftr-/- mice.
CONCLUSIONS:
Our findings point to an impaired adaptive homeotrophic liver response to prolonged hydrophobic bile salt exposure in CF conditions.
J Clin Invest. 2004 May;113(10):1408-18.
Bile acids lower triglyceride levels via a pathway involving FXR, SHP, and SREBP-1c.[Pubmed:
15146238 ]
METHODS AND RESULTS:
We explored the effects of bile acids on triglyceride (TG) homeostasis using a combination of molecular, cellular, and animal models. Cholic acid (CA) prevents hepatic TG accumulation, VLDL secretion, and elevated serum TG in mouse models of hypertriglyceridemia. At the molecular level, CA decreases hepatic expression of SREBP-1c and its lipogenic target genes. Through the use of mouse mutants for the short heterodimer partner (SHP) and liver X receptor (LXR) alpha and beta, we demonstrate the critical dependence of the reduction of SREBP-1c expression by either natural or synthetic farnesoid X receptor (FXR) agonists on both SHP and LXR alpha and LXR beta.
CONCLUSIONS:
These results suggest that strategies aimed at increasing FXR activity and the repressive effects of SHP should be explored to correct hypertriglyceridemia.
Toxicol Lett. 2014 Oct 17;232(1):246-252.
Diet supplementation with cholic acid promotes intestinal epithelial proliferation in rats exposed to γ-radiation.[Pubmed:
25455456]
Consumption of a high-fat diet increases some secondary bile acids (BAs) such as deoxyCholic acid (DCA) in feces. DCA is derived from Cholic acid (CA), a primary BA.
METHODS AND RESULTS:
We evaluated intestinal epithelial proliferation and BA metabolism in response to oral administration of Cholic acid (CA) in rats to determine the influence of a CA diet on the responses of gut epithelia to γ-rays. WKAH/HkmSlc rats were divided into two dietary groups: control diet or CA-supplemented (2g/kg diet) diet. Some of the rats from each group were irradiated with γ-rays, and epithelial cell proliferation in the colon was analyzed histochemically. Unirradiated CA-fed rats had high levels of DCA and CA in the sera, as well as the presence of tauroCholic acid in their feces. Significant increases were observed in both epithelial proliferation and the number of epithelial cells in the colon of the CA-fed rats, and this effect was observed at 8 weeks after γ-ray exposure. Furthermore, extracts from both cecal contents and sera of the unirradiated CA-fed rats promoted proliferation of IEC-6 cells.
CONCLUSIONS:
These results indicate that BAs in enterohepatic circulation promote proliferation and survival of the intestinal epithelium after receiving DNA damage.
