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. 2018 Jul 14;59(9):1695–1708. doi: 10.1194/jlr.M087056

Fig. 8.

Fig. 8.

Loss of intestinal CTα enhances biliary bile acid secretion. Gallbladders of male control and CTαIKO mice were cannulated, and bile was collected in preweighed containers (n = 6–8 per group). A: Bile flow. B: Bile salt secretion. C: Phospholipid secretion. D: Cholesterol secretion. E: Jejunal Lpcat4 expression. F: Relative biliary bile acid composition. G: Bile acid hydrophobicity index. H: Plasma bile acids. I: mRNA abundance of hepatic genes involved in bile acid synthesis. J: Fecal bile acids. mRNA abundance of jejunal bile-acid responsive genes (K) (n ≥ 4 per group) and mRNA abundance of ileal bile acid-responsive genes in control and CTαIKO mice 2 h after refeeding the HFD (L) (n = 3 per group). Values are means ± SEM. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. Β-MCA, β-β-muricholic acid; CA, cholic acid; Cyp7a1, cytochrome P450, family 7 subfamily a member 1; Cyp8b1, cytochrome P450, family 8 subfamily b member 1; Cyp27a1, cytochrome P450, family 27 subfamily a member 1; Fabp6, FA binding protein 6; Nrob2, nuclear receptor subfamily 0 group b member 2; TA-MCA, tauro-α-muricholic acid; TB-MCA, tauro-β-muricholic acid; TCA, taurocholic acid; TCDCA, taurochenodeoxycholic acid; THDCA, taurohyodeoxycholic acid; TUDCA, tauroursodeoxycholic acid.