|Description:||1. Chenodeoxycholic acid modulates GLP-1 and CCK secretion.|
2. Chenodeoxycholic acid is more likely to induce IL-8 production in vivo, especially under weakly acid conditions.
3. Chenodeoxycholic acid could reverse obesity in cHF-fed mice, mainly in response to the reduction in food intake.
4. Chenodeoxycholic acid can reduce the activity of cholesterol 27-hydroxylase - the first step in the acidic pathway for bile acid synthesis.
|Targets:||IL Receptor | p38MAPK | PKA|
|Source:||From the bile.|
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||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.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.5473 mL||12.7366 mL||25.4732 mL||50.9463 mL||63.6829 mL|
|5 mM||0.5095 mL||2.5473 mL||5.0946 mL||10.1893 mL||12.7366 mL|
|10 mM||0.2547 mL||1.2737 mL||2.5473 mL||5.0946 mL||6.3683 mL|
|50 mM||0.0509 mL||0.2547 mL||0.5095 mL||1.0189 mL||1.2737 mL|
|100 mM||0.0255 mL||0.1274 mL||0.2547 mL||0.5095 mL||0.6368 mL|
J Inherit Metab Dis. 2014 Sep;37(5):851-61.
|Liver disease in infancy caused by oxysterol 7 α-hydroxylase deficiency: successful treatment with chenodeoxycholic acid.[Pubmed: 24658845]|
|On treatment with ursodeoxycholic acid (UDCA), his condition was worsening, but on Chenodeoxycholic acid (CDCA), 15 mg/kg/d, he improved rapidly. A biopsy (after 2 weeks on Chenodeoxycholic acid ), showed a giant cell hepatitis, an evolving micronodular cirrhosis, and steatosis. The improvement in liver function on Chenodeoxycholic acid was associated with a drop in the plasma concentrations and urinary excretions of the 3β-hydroxy-Δ5 bile acids which are considered hepatotoxic. At age 5 years (on Chenodeoxycholic acid , 6 mg/kg/d), he was thriving with normal liver function. Neurological development was normal apart from a tendency to trip. Examination revealed pes cavus but no upper motor neuron signs. The findings in this case suggest that Chenodeoxycholic acid can reduce the activity of cholesterol 27-hydroxylase - the first step in the acidic pathway for bile acid synthesis.|
Int J Obes (Lond). 2014 Aug;38(8):1027-34.
|Enhancement of brown fat thermogenesis using chenodeoxycholic acid in mice.[Pubmed: 24310401 ]|
|In this study, the effects of another natural BA, Chenodeoxycholic acid (CDCA), on dietary obesity, UCP1 in both interscapular BAT and in white adipose tissue (brite cells in WAT), were characterized in dietary-obese mice. RESEARCH DESIGN: Mice were then fed either (i) for 8 weeks with cHF or with cHF with two different doses (0.5%, 1%; wt wt(-1)) of Chenodeoxycholic acid (8-week reversion). RESULTS: In the 8-week reversion, the Chenodeoxycholic acid intervention resulted in a dose-dependent reduction of obesity, dyslipidaemia and glucose intolerance, which could be largely explained by a transient decrease in food intake. The 3-week reversion revealed mild Chenodeoxycholic acid-dependent and food intake-independent induction of UCP1-mediated thermogenesis in interscapular BAT, negligible increase of UCP1 in subcutaneous WAT and a shift from carbohydrate to lipid oxidation. CONCLUSIONS: Chenodeoxycholic acid could reverse obesity in cHF-fed mice, mainly in response to the reduction in food intake, an effect probably occuring but neglected in previous studies using cholic acid. Nevertheless, Chenodeoxycholic acid-dependent and food intake-independent induction of UCP1 in BAT (but not in WAT) could contribute to the reduction in adiposity and to the stabilization of the lean phenotype.|
J Gastroenterol Hepatol. 2013 May;28(5):823-8.
|Acidic deoxycholic acid and chenodeoxycholic acid induce interleukin-8 production through p38 mitogen-activated protein kinase and protein kinase A in a squamous epithelial model.[Pubmed: 23425072]|
|Conjugated bile acids under a neutral or acidic condition did not induce IL-8 production, and unconjugated bile acids, deoxycholic acid (DCA), and Chenodeoxycholic acid (CDCA) all significantly induced IL-8 production, dose- and time-dependently, only under weakly acid conditions. Inhibition of p38 mitogen-activated protein kinase (p38 MAPK) and protein kinase A (PKA) attenuated the production of IL-8 induced by acidic DCA and Chenodeoxycholic acid. Inhibition of PKA did not block the bile acid-induced p38 MAPK activation. CONCLUSIONS: Compared with conjugated bile acids, the unconjugated bile acids DCA and Chenodeoxycholic acid are more likely to induce IL-8 production in vivo, especially under weakly acid conditions. This process involves two independent signaling pathways, p38 MAPK and PKA.|
J Clin Endocrinol Metab. 2013 Aug;98(8):3351-8.
|Effects of chenodeoxycholic acid on the secretion of gut peptides and fibroblast growth factors in healthy humans.[Pubmed: 23783097]|
|We hypothesized that intraduodenal infusions of Chenodeoxycholic acid (CDCA) would stimulate FGF and gut peptide secretion, thereby positively influencing glucose homeostasis. DESIGN, SETTING, PARTICIPANTS, AND INTERVENTION: This randomized, double-blind, placebo-controlled, crossover trial included 12 healthy volunteers who received intraduodenal infusions (2.0 mL/min for 180 minutes) of saline, Chenodeoxycholic acid (5 or 15 mmol/L), and a fatty acid (sodium oleate), either alone or with 5 mmol/L Chenodeoxycholic acid. After 60 minutes, an oral glucose tolerance test (oGTT) was performed. RESULTS: Within the first 60 minutes, high-concentration Chenodeoxycholic acid induced a small but significant increase in GLP-1 and CCK secretion (P = .016 and P =.011), whereas plasma C-peptide, insulin, and glucose were not affected. Attenuated C-peptide and insulin release was observed after the oGTT with 15 mmol/L CDCA (P = .013 and P =.011). Plasma BA and FGF19 levels significantly increased after Chenodeoxycholic acid administration (P = .001 and P < .001). CONCLUSIONS: Chenodeoxycholic acid modulates GLP-1 and CCK secretion; the effect is small and does not influence glucose levels. The marked increase in plasma BAs and the attenuated insulin release after the oGTT indicate the role of BAs in glycemic control, independent of the incretin axis, and suggest involvement of farnesoid X receptor activation pathways.|