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Fecal metabolomic response of IL‐10‐deficient mice supplemented with Goji
Author(s) -
Wang Hongbin,
Zhang Shuming,
Zhu Meijun
Publication year - 2019
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.2019.33.1_supplement.723.1
Subject(s) - polyunsaturated fatty acid , linoleic acid , eicosapentaenoic acid , food science , bifidobacterium , gut flora , biology , feces , chemistry , biochemistry , fatty acid , lactobacillus , microbiology and biotechnology , fermentation
Background Chronic gut inflammation is an important risk factor for colorectal cancer (CRC). Our recent study suggests that dietary Goji reduces gut inflammation and increases Bifidobacterium and butyrate‐producing bacteria in interleukin (IL)‐10‐deficient mice. We hypothesized that enhanced Bifidobacterium and other probiotics associated with Goji supplementation alter gut metabolites, which exert beneficial effects to host epithelial cells. Methods The GC‐MS analysis was used to profile the fecal metabolomic changes due to Goji supplementation to uncover the potential mechanisms underlying the preventive effects of Goji supplementation on inflammatory bowel diseases. Results Thirty‐four compounds were altered due to Goji supplementation, including polyunsaturated long‐chain fatty acids (PUFAs), sugar and sugar alcohols, benzene derivatives, pyridines derivatives, dicarboxylic acids, short‐chain hydroxy acids. Pathway analysis showed that the α‐linolenic acid and linoleic acid metabolism were dramatically affected by dietary Goji intake. Four ω‐6 PUFAs including linoleic acid and arachidonic acid were reduced due to Goji supplementation. Fecal levels of most amino acids, positively correlated with gut inflammation and CRC risk, tended to decrease in the Goji supplemented group along with decreased urease activity. Conclusion data provides valuable metabolic clues for unravelling the beneficial effects of Goji supplementation against gut inflammation and related diseases. Support or Funding Information USDA‐NIFA #2018‐67017‐27517 and WSU ERI competitive grant This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .