PuSH - Publication Server of Helmholtz Zentrum München

Fujisaka, S.* ; Avila-Pacheco, J.* ; Soto, M.* ; Kostic, A.* ; Dreyfuss, J.M.* ; Pan, H.* ; Ussar, S. ; Altindis, E.* ; Li, N.* ; Bry, L.* ; Clish, C.B.* ; Kahn, C.R.*

Diet, genetics, and the gut microbiome drive dynamic changes in plasma metabolites.

Cell Rep. 22, 3072-3086 (2018)
Publ. Version/Full Text Postprint Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Diet, genetics, and the gut microbiome are determinants of metabolic status, in part through production of metabolites by the gut microbiota. To understand the mechanisms linking these factors, we performed LC-MS-based metabolomic analysis of cecal contents and plasma from C57BL/6J, 129S1/SvImJ, and 129S6/SvEvTac mice on chow or a high-fat diet (HFD) and HFD-treated with vancomycin or metronidazole. Prediction of the functional metagenome of gut bacteria by PICRUSt analysis of 16S sequences revealed dramatic differences in microbial metabolism. Cecal and plasma metabolites showed multifold differences reflecting the combined and integrated effects of diet, antibiotics, host background, and the gut microbiome. Eighteen plasma metabolites correlated positively or negatively with host insulin resistance across strains and diets. Over 1,000 still-unidentified metabolite peaks were also highly regulated by diet, antibiotics, and genetic background. Thus, diet, host genetics, and the gut microbiota interact to create distinct responses in plasma metabolites, which can contribute to regulation of metabolism and insulin resistance.
Altmetric
Additional Metrics?
[➜Log in]
Edit extra informations Login
Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Antibiotics ; Bile Acids ; Cecal Metabolomics ; Diabetes ; Diet ; Gut Microbiome ; Obesity ; Serum Lipids ; Serum Metabolomics ; Tmao; Chain Fatty-acids; Insulin-resistance; Obese Mice; Disease; Risk; Health; Phosphatidylcholine; Contributes; Sensitivity; Physiology
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Journal Cell Reports
Quellenangaben Volume: 22, Issue: 11, Pages: 3072-3086 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes and Obesity (IDO)