期刊
SURGERY
卷 144, 期 2, 页码 174-181出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.surg.2008.03.035
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资金
- NCRR NIH HHS [P40 RR018603-03, P40 RR018603] Funding Source: Medline
- NIDDK NIH HHS [P30 DK34987, P30 DK034987-22, P30 DK034987, R01 DK083325] Funding Source: Medline
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 marine 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-tinge polymerase chain reaction (RTPCR) 7 days following surgery. Results. Following ICR WT mice showed significant increases in the expression of genes regulating bile acid transport including IBABP, Asbt, Ost beta 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.
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