Bile acid (BA) conjugation deficiency and altered BA metabolism in bile acid‐CoA: amino acid N‐acyltransferase (Baat
−/−
) mice. Ten‐week‐old mice fed chow were sacrificed after overnight fasting for the following BA and gene‐expression analysis. (A) Hepatic BA composition was determined using liquid chromatography–mass spectrometry (LC/MS). Among identified 25 BAs, 20 unconjugated BAs and their tauro‐conjugated counterparts were presented with average ± SEM (n = 5). Glycoconjugated BAs[
5
] were omitted because of their extremely low levels. Each panel contains unconjugated BAs (left) and their corresponding tauro‐conjugated BAs (right). (B) Biliary BA composition was determined using LC/MS as described in (A). (C) Unconjugated and tauro‐conjugated BA levels of liver, gallbladder (GB), plasma, and ileum (from left to right) calculated from the LC/MS analysis are plotted as absolute values. (D) Gene expression was quantified using quantitative polymerase chain reaction (PCR) analysis for hepatic BA homeostasis (top panel), hepatobiliary transporters (bottom left panel), and intestinal BA metabolism (bottom right panel). *p < 0.05, **p < 0.01, ***p < 0.005. CA, cholic acid; Cyp7a1, cholesterol 7α‐hydroxylase; Cyp8b1, sterol 12α‐hydroxylase; DCA, deoxycholic acid; Fatp2, fatty acid transport protein 2; Fgf15, fibroblast growth factor 15; FXR, farnesoid X receptor; HCA, hyocholic acid; HDCA, hyodeoxycholic acid; Ibabp, ileal bile acid‐binding protein; LCA, lithocholic acid; MCA, muricholic acid; Ostb, organic solute transporter β; Shp, small heterodimer partner; TCA, trichloroacetic acid; TCDCA, taurochenodeoxycholic acid; TDCA, taurodeoxycholic acid; TDHCA, taurodehydrocholic acid; THCA, tetrahydrocannabinolic acid; TLCA, taurolithocholic acid; TUDCA, tauroursodeoxycholic acid; UDCA, ursodeoxycholic acid; WT, wild type.