Only free bile acid drives ileal absorption of taurocholate

We compared the intestinal absorption of monomeric taurocholate bound to albumin with the absorption of the free form. In the presence of albumin the apparent uptake coefficient is about three times greater than that in its absence. This result resembles the one reported previously for the liver. In the gut, however, this phenomenon is attributable to the diffusive resistance of an unstirred intervillous fluid layer, whereas in the liver this explanation has been excluded. We conclude that only free taurocholate engages the bile acid transport system in ileal mucosa, whereas in the liver bile acid uptake is driven by albumin-taurocholate complexes, as well as by free taurocholate.

Synthesis of bile acid monosulphates by the isolated perfused rat kidney

Perfusion of an isolated rat kidney with labelled bile acids, in a protein-free medium, resulted in the urinary excretion of the labelled bile acid, 3% being converted into polar metabolities in 1h. These metabolities were neither glycine nor taurine conjugates, nor bile acid glucuronides, and on solovolysis yielded the free bile acid. On t.l.c. the metabolite of [24-14C]lithocholic acid had the mobility of lithocholate 3-sulphate. The principal metabolite of [24-14C]chenodeoxycholic acid had the mobility of chenodeoxycholate 7-sulphate; trace amounts appeared as chenodeoxycholate 3-sulphate. [35S]sulphate was incorporated in chenodeoxycholic acid by the kidney, resulting in a similar pattern of sulphation. No disulphate salt of chenodeoxycholic acid was detected. These findings lend support to the hypothesis that renal synthesis may account for some of the bile acid sulphates present in urine in the cholestatic syndrome in man.