Bacterial-dependent up-regulation of intestinal bile acid binding protein and transport is FXR-mediated following ileo-cecal resection
Autor: | Aaron P. Garrison, Susan J. Henning, Rachael Rigby, Douglas C. von Allmen, Christopher M. Dekaney, Michael A. Helmrath, P. Kay Lund |
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Jazyk: | angličtina |
Rok vydání: | 2008 |
Předmět: |
Male
medicine.medical_specialty Organic anion transporter 1 medicine.drug_class Colon animal diseases Organic Anion Transporters Sodium-Dependent Receptors Cytoplasmic and Nuclear Ileum Biology Article Bile Acids and Salts Cecum Mice Downregulation and upregulation Internal medicine Gene expression medicine Animals Germ-Free Life Receptor Bile acid Symporters Hydroxysteroid Dehydrogenases virus diseases Biological Transport Up-Regulation DNA-Binding Proteins Mice Inbred C57BL medicine.anatomical_structure Endocrinology Symporter biology.protein Surgery Transcription Factors |
DOI: | 10.17615/7b9g-r479 |
Popis: | Background Bile acid (BA) reclamation following ileo-cecal resection (ICR) may prevent colonic mucosa from chronic injury. In this study, we hypothesized that in a murine model of ICR the remnant colon would upregulate the cellular machinery necessary for BA reclamation and would do so in an FXR- and bacteria-dependent manner. Methods Conventional (WT), conventional FXR knockout (FXR null) and germ-free (GF) mice were randomized to undergo either ICR or sham operation. The ascending colon was harvested for histology and immunohistochemistry and changes in bile acid homeostatic gene expression determined by real-time polymerase chain reaction (RT-PCR) 7 days following surgery. Results Following ICR WT mice showed significant increases in the expression of genes regulating bile acid transport including IBABP, Asbt, Ostβ and FGF 15. Increased expression of IBABP and Asbt was confirmed by immunohistochemistry. Induction of bile acid transport genes was absent or attenuated in FXR null and GF mice. Conclusion Bacterial dependent up regulation of IBABP is FXR mediated in the colon following ICR. Mice lacking microbiota (GF) or FXR are unable to increase the expression of IBABP or FGF 15. |
Databáze: | OpenAIRE |
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