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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)
Verlagsversion Postprint Forschungsdaten 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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Sprache englisch
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 22, Heft: 11, Seiten: 3072-3086 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
POF Topic(s) 30502 - Diabetes: Pathophysiology, Prevention and Therapy
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-508600-009
DOI 10.1016/j.celrep.2018.02.060
WOS ID WOS:000427493400022
Scopus ID 85043592218
PubMed ID 29539432
Erfassungsdatum 2018-05-24
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