Fig. 12.

Summary figure depicting the consequences of PHx on bile acid homeostasis and transporters in mice. Arrows represent changes from wild-type mice for a metabolite, enzyme, or transporter. PHx does not significantly influence the hepatic concentrations of taurine-conjugated BAs and, consequently, the concentrations of total BAs in the liver. However, the glycine and unconjugated BA concentrations increase significantly in liver. To maintain BA concentrations after PHx, the remnant liver, besides decreasing bile acid de novo synthesis (Cyp7a, 8b1, 27a1), increases the BA efflux into bile, probably via increasing Bsep activity. After PHx, hepatocytes also limit the accumulation of BAs by upregulating basolateral efflux transporters, including Mrp3 and Ostα/β. Probably owing to this aforementioned induction of transporters, the plasma concentrations of unconjugated, glycine-, and taurine-conjugated BAs increase. The biliary tree is likely protected against the harmful effects of enhanced bile acid excretion by Mdr2, which can be responsible for enhanced canalicular excretion of phospholipids. Conj, conjugated.