Disease relevance of Chenodiol

• The gallstone index of the bacterium-treated group was lower than that of CDCA-treated group during the period of experiment, but there was no difference in the cholesterol content of gallstones between these two groups, which suggests a different mechanism of action of the bacterium from that of CDCA [1].
• The effect of oral administration of Clostridium butyricum Miyairi on the formation and dissolution of gallstones was examined in a mouse model of cholesterol cholelithiasis, in comparison with that of chenodeoxycholic acid (CDCA) [1].

High impact information on Chenodiol

• Human primary hepatocytes and HepG2 cells were used as models to study chenodeoxycholic acid (CDCA) and interleukin-1 beta (IL-1 beta) regulation of human CYP7A1 gene expression via real-time polymerase chain reaction, reporter assays, co-immunoprecipitation and chromatin immunocipitation (ChIP) assays [2].
• Feedback regulation of bile acid synthesis in primary human hepatocytes: evidence that CDCA is the strongest inhibitor [3].
• We further demonstrate that CDCA stabilizes LDL receptor mRNA and that the MAP kinase inhibitors accelerate its turnover [4].
• On the other hand, inhibition of mitogen-activated protein (MAP) kinase activities, which are found to be induced by CDCA, abolishes the CDCA-mediated up-regulation of LDL receptor gene expression [4].
• The concentration of CDCA required to inhibit 50% of reporter activity (IC(50)) was determined to be approximately 25 microM without FXR and 10 microM with FXR [5].

Anatomical context of Chenodiol

• In the presence of calcium and phosphate, CDCA induced the permeability transition pore (PTP) in freshly isolated rat liver mitochondria [6].

Gene context of Chenodiol

• IL-1 beta and CDCA reduced CYP7A1 but induced c-Jun messenger RNA expression in human primary hepatocytes [2].

References