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Metabolomic and Clinical Disturbances in Canine Inflammatory Bowel Disease
Author(s) -
Jackson Matthew,
Jewell Dennis
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.265.7
Subject(s) - medicine , inflammatory bowel disease , metabolome , ulcerative colitis , disease , metabolomics , gastroenterology , enteropathy , dysbiosis , etiology , immunology , physiology , biology , bioinformatics , metabolite
Canine inflammatory bowel disease (IBD) is a progressive disease with poorly characterized etiology. We sought to gain insight into the metabolic disturbances preceding and co‐incident with canine IBD by comparing the plasma metabolome and clinical indices of dogs (n =30) prior and subsequent to diagnosis of IBD by histopathological assessment of intestinal tissue collected by endoscopy. Archived samples were generated from annual health screens and adventitious health‐related collections curated according to the IBD status of their donors. Metabolomic and clinical analysis was also performed on bioarchived time‐matched samples from disease‐free, healthy control dogs (n = 30). Blood collections were carried out under IACUC approved protocols. Results showed several circulating metabolites of colon microbiota were decreased in IBD dogs, including phenol and indole derivatives. Further disruptions were noted in antioxidant status and lipid metabolism. A stepwise discriminant model selected a subset of clinical markers including liver enzymes, plasma and urine protein, platelets, basophils and monocytes as capable of correctly classifying >90% of samples as derived from post‐IBD versus healthy controls. The clinical findings imply that disruption of the gut and liver barriers, protein‐losing enteropathy and immune perturbation was co‐incident with IBD. In summary, assessment of dogs pre‐, peri‐ and post‐diagnosis implies hindgut dysbiosis, altered redox status and disrupted lipid metabolism accompany clinical disturbances in canine IBD.