Deletion of the Casp8 gene in mice results in ileocolitis, gut barrier dysfunction, and malassimilation, which can be partially attenuated by inulin or sodium butyrate.
Günther C, Kaden-Volynets V, Zimmermann J, Beisner J, Becker C, Bischoff SC (2019)
Publication Language: English
Publication Status: Published
Publication Type: Journal article
Publication year: 2019
Journal
Book Volume: 317
Pages Range: G493-G507
Journal Issue: 4
Abstract
Genetic mouse models for ileocolitis are important to understand inflammatory bowel disease in humans. We examined dietetic factors that might aggravate or attenuate ileocolitis and related pathologies in such a model. Deletion of the caspase-8 gene results not only in ileocolitis but also in gut barrier dysfunction, liver steatosis, and malassimilation, which can be partially attenuated by oral inulin or sodium butyrate. Our data indicate that diet modifications can contribute to disease variability and therapy.
Authors with CRIS profile
Claudia Günther
Professur für Gastrointestinale Pathophysiologie
Julia Zimmermann
Lehrstuhl für Innere Medizin III
Christoph Becker
Professur für Molekulare Gastroenterologie
Involved external institutions
Germany (DE)How to cite
APA:
Günther, C., Kaden-Volynets, V., Zimmermann, J., Beisner, J., Becker, C., & Bischoff, S.C. (2019). Deletion of the Casp8 gene in mice results in ileocolitis, gut barrier dysfunction, and malassimilation, which can be partially attenuated by inulin or sodium butyrate. American Journal of Physiology-Gastrointestinal and Liver Physiology, 317(4), G493-G507. https://doi.org/10.1152/ajpgi.00297.2018
MLA:
Günther, Claudia, et al. "Deletion of the Casp8 gene in mice results in ileocolitis, gut barrier dysfunction, and malassimilation, which can be partially attenuated by inulin or sodium butyrate." American Journal of Physiology-Gastrointestinal and Liver Physiology 317.4 (2019): G493-G507.
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