bile acid


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Related to bile acid: bile salt

bile acid

/bile ac·id/ (bīl as´id) any of the steroid acids derived from cholesterol; classified as primary, those synthesized in the liver, e.g., cholic and chenodeoxycholic acids, or secondary, those produced from primary bile acids by intestinal bacteria, e.g., deoxycholic and lithocholic acids. Most of the the bile acids are reabsorbed and returned to the liver via the enterohepatic circulation. Cf. bile salt under salt.

bile acid

n.
Any of the liver-generated steroid acids, such as cholic acid, that commonly occur in the bile in combination with glycine and taurine as sodium salts.

bile acid

a steroid acid of the bile, produced during the metabolism of cholesterol. On hydrolysis, bile acid yields glycine and choleic acid.

bile acid

Either of several acids—e.g., cholic acid (CA), chenodeoxycholic acid (CDA)—which are formed in the liver and converted by intestinal bacteria into deoxycholic acid (from CA) and lithocholic acid (from CDA), which are known as secondary BAs. BAs are conjugated in the liver to glycine or taurinese conjugates; glycocholic acid and taurocholic acid form sodium and potassium salts in the alkaline bile in the liver. These conjugated bile acids have a central role in the emulsification and absorption of fatty acids.

Specimen
Serum.
 
Ref range
< 60 µg/mL—as cholylglycine.
 
Method
RIA.
References in periodicals archive ?
The data generated from this group revealed that the reduced hepatic inflammation by antibiotics was accompanied by decreased free and conjugated secondary bile acids in a gender-dependent manner.
Intrahepatic cholestasis of pregnancy: changes in maternal-fetal bile acid balance and improvement by ursodeoxycholic acid.
16 Non availability of bile acids was a major limitation of our study but we adopted a pragmatic approach and diagnosed ICP like presently we are doing in our clinical setting by clinical features and excluding other causes.
The toxic effect of bile acids is well documented [21, 29, 30] and accumulation in the liver is one of the main factors associated with cholestasis.
FAB-MS, however, is not an accepted technique for accurate quantification but does provide a semiquantitative assessment of the relative concentrations of the atypical bile acids excreted in patients with genetic defects in bile acid synthesis.
Conclusion: The increased biliary content and fecal excretion of bile acids and sterols in our study suggest that the dietary water-soluble gunny fiber of S.
Gut microbiota regulates bile acid metabolism by reducing the levels of taurobeta-muricholic acid, a naturally occurring FXR antagonist.
Overexpression of cholesterol 7[alpha]-hydroxylase promotes hepatic bile acid synthesis and secretion and maintains cholesterol homeostasis.
Taurine reduces bilirubin, total bile acids, and biliary glycine:taurine ratio within one week in patients with hepatitis as compared to controls.
By selectively elevating BSH levels in conventionally raised mice with a normal microbiota, the study demonstrated BSH can modify plasma bile acid profiles which can influence pathways governing lipid metabolism, metabolic signalling events, circadian rhythm and immune function.
In vitro assay has been widely accepted to estimate the potential bile acid binding capacity of polysaccharides including CS.