Biohydrogenation of A5-steroids was studied in vitro by incubating various steroids with a pure culture of Eubacterium 21,408 in a brain-thioglycollat

SUMMARY Samples of serum, bile, and urine were collected simultaneously from patients with cholestasis of varying aetiology and from patients with cirrhosis; their bile acid composition was determined by gas/liquid chromatography and mass spectrometry In cholestasis, the patterns in all three body fluids differed consistently and strikingly. In serum, cholic acid was the major bile acid and most bile acids (> 93 %) were unsulphated, whereas, in urine, chenodeoxycholic was the major bile acid, and the majority of bile acids (> 60 %) were sulphated. Secondary bile acids were virtually absent in bile, serum, and urine. The total amount of bile acids excreted for 24 hours correlated highly with the concentration of serum bile acids; in patients with complete obstruction, urinary excretion averaged 71 6 mg/24 h. In cirrhotic patients, serum bile acids were less raised, and chenodeoxycholic acid was the predominant acid. In healthy controls, serum bile acids were consistently richer in chenodeoxycholic acid than biliary bile acids, and no bile acids were present in urine. No unusual monohydroxy bile acids were present in patients with primary biliary cirrhosis, but, in several patients, there was a considerable amount of hyocholic acid present in the urinary bile acids. The analyses of individual bile acids in serum and urine did not appear to provide helpful information in the differential diagnosis of cholestasis. Thus, in cholestasis, conjugation of chenodeoxycholic acid with sulphate becomes a major biochemical pathway, urine becomes a major route of bile acid excretion, and abnormal bile acids are formed.

Sulfated and non-sulfated bile acids were determined in the intestines and in the feces of 7-month-old germ-free and conventional male mice.1. The bile acid pools in the gall bladder and small intestine were 21.13 mg/100 g body weight in germ-free and 11.50 mg in conventional mice. The bile acid pools in the cecum and large intestine of germ-free mice were 3.03 mg/100 g body weight as compared to 1.24 mg in conventional mice. Fecal bile acid excretion was 2.93 mg and 4.12 mg/100 g body weight in 24 h in germ-free and conventional mice respectively.2. The major bile acids from germ-free mice were cholic acid, a-muricholic acid and P-muricholic acid. Small amounts of chenodeoxycholic and allocholic acid were also present. In addition to these primary bile acids the following secondary bile acids were identified in conventional mice : lithocholic, deoxycholic and co-muricholic acid.3. In both germ-free and conventional animals significant amounts of chenodeoxycholic and cholic acid were present as the 7-monosulfate esters. The sulfate esters of these bile acids did not exceed 2% of the total bile acids in the small intestine, but accounted for approximately 50% of the bile acids in the cecum and the large intestine. In contrast, the muricholic acids were nearly exclusively found in the non-sulfate fraction.4. Alkaline hydrolysis without prior solvolysis of the sulfate esters resulted in loss of bile acids and production of artifacts. Hence, the bile acids of the mouse cannot be analysed by methods involving alkaline deconjugation unless a solvolysis step is included in the procedure.Sulfation is an important pathway in bile acid metabolism when the enterohepatic circulation is partially or completely interrupted. In a variety of hepatobiliary diseases in man, significant amounts of sulfated bile acids are excreted in the urine [l -51. In contrast, sulfation of bile acids seems to be less pronounced in normal man. Although more than 50 % of the small quantity of lithocholic acid in normal human bile is sulfated [6], only minute amounts of the major dihydroxy and trihydroxy bile acids are excreted as sulfate esters in the bile or the urine of healthy subjects [2]. Similar data have been reported in studies on rats. Lithocholic acid is sulfated by the Trivial names. Lithocholic acid : 3cc-hydroxy-S~-cholan-24-oic acid; deoxycholic acid : 3a,l2a-dihydroxy-S~-cholan-24-oic acid; hyodeoxycholic acid : 3cc,6a-dihydroxy-S~-cholan-24-oic acid ; ursodeoxycholic acid : 3a,7P-dihydroxy-5~-cholan-24-oic acid; chenodeoxycholic acid : 3a,7n-dihydroxy-5~-cholan-24-oic acid ; cholic acid : 3a,7a,l2a-trihydroxy-S~-cholan-24-oic acid; allocholic acid : 3cc,7a,l2a-trihydroxy-5a-cholan-24-oic acid; oc-muricholic acid: 3cc, 6~,7a-trihydroxy-5~-cholan-24-oic acid; P-muricholic acid : 3oc,6p, 7~-trihydroxy-S~-cholan-24-oic acid; w -muricholic acid : 3c(.6a,7/-trihydroxy-5~-cholan-24-oic acid ; 23-nordeoxycholic acid : 3cc,12oc-dihydroxy-5~-cholan-23-oic acid. normal rat liver [7]. The sulfation rate of dihydroxy and trihydroxy bile acids ...

No abstract