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Impact of Diet and Genetic Induced Obesity on the Stool Metabolome of Tumor Prone Mice
Author(s) -
Nesbeth PaulaDene,
Pfalzer Anna,
Iyer Lakshmanan,
Parnell Laurence,
Liu Zhenhua,
Mason Joel,
Crott Jimmy
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.394.8
Subject(s) - metabolome , metabolomics , metabolite , medicine , endocrinology , colorectal cancer , metabolism , gluconeogenesis , bile acid , lipid metabolism , obesity , lipidomics , biology , biochemistry , cancer , bioinformatics
Obesity is associated with an increased risk of colorectal cancer. It is unclear whether this association is driven by metabolic interactions and adaptations to chronic high fat “Western Diet” exposure or excess adiposity. To expound on this association, we characterized the stool metabolome of tumor‐prone Apc 1638N made obese by high fat (HF) feeding or the presence of an obesogenic mutation (DbDb). Untargeted metabolomic profiling of stool identified 415 metabolites. Forty‐nine metabolites were significantly altered in HF mice and 41 metabolites in Dbdb mice compared to LF mice (P<0.05). Five metabolites were significantly lower in both comparisons to LF mice: arachidic acid, adenosine, caproic acid, 2‐oxindole‐3‐acetate, tyrosyl‐glycine. Pathway analysis showed changes pyruvate metabolism and gluconeogenesis (adj. P<0.05) identified by significant decreases in lactate and malate in HF compared to LF mice. Sphingosine, sphinganine, and secondary bile acid, lithocholate, were significantly reduced in Dbdb mice compared to LF indicating possible shifts in sphingolipid and bile acid metabolism. Differences in metabolite abundances in stool may identify novel biomarkers for diagnosis, and targets for treatment and prevention of obesity‐induced colorectal cancer.