Disease relevance of C01558

• Bile salt sensitivity of Escherichia coli chi1776 [1].
• Bile acid synthesis by long-term cultured cell line established from human hepatoblastoma [2].
• Bile salt kinetics in cystic fibrosis: influence of pancreatic enzyme replacement [3].
• Bile acid synthesis is increased in Chilean Hispanics with gallstones and in gallstone high-risk Mapuche Indians [4].
• Bile salt malabsorption in pancreatic insufficiency secondary to alcoholic pancreatitis [5].

Psychiatry related information on C01558

• Bile acid concentrations in serum, and urinary and faecal excretion of bile acids have been studied in ten patients with liver cirrhosis as a consequence of alcohol abuse [6].

High impact information on C01558

• Bile acid regulation of gene expression: roles of nuclear hormone receptors [7].
• Bile acid-activated nuclear receptor FXR suppresses apolipoprotein A-I transcription via a negative FXR response element [8].
• Multiple studies have now shown that, although supraphysiological doses of the bile acid taurocholic acid can suppress human apolipoprotein A-1 (apoA-1) transcription in human apoA-1 transgenic mice this suppression is not mediated via FXR [9].
• Bile acid kinetics were determined with cholic and chenodeoxycholic acids labeled with carbon13, by measuring the relative abundance of 13C in duodenal bile acids for 4--5 d [10].
• Bile acid-induced increase in bile acid-independent flow and plasma membrane NaK-ATPase activity in rat liver [11].
• The effects of intraduodenal glycerol, fatty acid (FA) chain length and FA loads, and bile acid (BA) concentrations on pancreatic and gallbladder function were investigated in 31 healthy volunteers by a perfusion method [12].

Chemical compound and disease context of C01558

• CONCLUSIONS: Bile acid concentrations are elevated and cholic acid is the major species accumulating in colostrum, reflecting serum bile acid profiles in intrahepatic cholestasis of pregnancy [13].
• An infusion of increasing amounts of the hydrophobic BS taurodeoxycholate increased cholesterol excretion by 3.0- and 2.4-fold in wild-type and Abcg5(-/-) mice but rapidly induced cholestasis in Abcg5(-/-) mice [14].
• Taurine seems to be essential in the newborn for bile acid (BA) tauroconjugation, and its deficiency has been implicated in total parenteral nutrition-associated cholestasis (TPN-AC) [15].

Biological context of C01558

• BACKGROUND & AIMS: Bile salt-induced apoptosis is mediated by a trypsin-like nuclear protease [16].
• RESULTS: Bile acid treatment of primary rat hepatocytes prevented retinoid activation of ntcp gene expression and function; this corresponded temporally with shp gene activation [17].
• Bile acid-mediated down-regulation occurred via fxr-dependent suppression of the ntcp RXR:RAR response element [17].
• Bile acid output and the interdigestive migrating motor complex in normals and in cholecystectomy patients [18].
• CONCLUSIONS: Bile acid synthesis in humans has a diurnal rhythm, with 2 peaks during the daytime, that is opposite from the circadian rhythm of cholesterol synthesis [19].

Anatomical context of C01558

• Higher BA concentrations exerted an opposite effect, slowing FA absorption and increasing pancreatic and gallbladder responses [12].
• Bile acid concentrations in human and rat liver tissue and in hepatocyte nuclei [20].
• Bile acid compositions in the serum, urine, bile, and feces were examined in a typical case of benign recurrent intrahepatic cholestasis for a period of 3 yr [21].
• Bile acid transport by basal membrane vesicles of human term placental trophoblast [22].
• Bile acid output in the duodenum was studied in relation to the interdigestive migrating motor complex in normal subjects and in cholecystectomy patients [18].

Associations of C01558 with other chemical compounds

• Bile acid synthesis by cultured hepatocytes. Inhibition by mevinolin, but not by bile acids [23].
• RESULTS: Bile acid perfusion did not significantly alter stimulated pancreatic enzyme, bilirubin or bile acid output or plasma CCK [24].
• Bile acid breath tests and lactose tolerance tests were not, however, reliable indicators of jejunal bacterial overgrowth [25].
• The presence of a hydroxy group at the C-23 position increased the acidity of the BA and this accounted for poor absorption within the biliary tree and efficient biliary secretion without the need for conjugation [26].
• These experiments are consistent with the hypothesis that sn-1 palmitoyl L species are subselected for bile, in part, by physical-chemical interactions of intracellular BS concentrations with Ch-poor membranes and that the subsequent evolution of Ch-rich vesicles and Ch-saturated mixed micelles occurs via a transitional hexagonal (rod) phase [27].

Gene context of C01558

• Bile acid-induced activation of activator protein-1 requires both extracellular signal-regulated kinase and protein kinase C signaling [28].
• Bile acid transport in sister of P-glycoprotein (ABCB11) knockout mice [29].
• Bile acid synthesis in Cyp7a1(+/+) males and females was increased 2-fold by cholesterol feeding, and 4-fold by cholestyramine treatment, but was not changed in matching Cyp7a1(-/-) mice by either of these manipulations [30].
• Bile acid signaling through FXR induces intracellular adhesion molecule-1 expression in mouse liver and human hepatocytes [31].
• Bile acid-induced alterations of mucin production in differentiated human colon cancer cell lines [32].

Analytical, diagnostic and therapeutic context of C01558

• Bile acid synthesis was determined using HPLC based on mass or by isotope dilution [33].
• Bile salt deconjugation breath tests [34].
• RESULTS: Bile acid quantity and concentration in the gastric aspirates were significantly greater in Billroth II subjects than in total biliary diversion subjects [35].
• Bile acid conjugation in organ culture of human fetal liver [36].
• METHODS: Bile acid transport activity and ecto-ATPase expression were analyzed in primary rat hepatocytes, rat hepatoma HTC cells, and specially adapted HTC (HTC-R) cells using plasma membrane vesicles and Northern blot, slot blot, ribonuclease protection assay, and Western blot analyses [37].

References