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Kindt, A. ; Liebisch, G.* ; Clavel, T.* ; Haller, D.* ; Hörmannsperger, G.* ; Yoon, H.* ; Kolmeder, D.* ; Sigruener, A.* ; Krautbauer, S.* ; Seeliger, C.* ; Ganzha, A.* ; Schweizer, S.* ; Morisset, R.* ; Strowig, T.* ; Daniel, H.* ; Helm, D.* ; Küster, B.* ; Krumsiek, J. ; Ecker, J.R.*

The gut microbiota promotes hepatic fatty acid desaturation and elongation in mice.

Nat. Commun. 9:3760 (2018)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Interactions between the gut microbial ecosystem and host lipid homeostasis are highly relevant to host physiology and metabolic diseases. We present a comprehensive multiomics view of the effect of intestinal microbial colonization on hepatic lipid metabolism, integrating transcriptomic, proteomic, phosphoproteomic, and lipidomic analyses of liver and plasma samples from germfree and specific pathogen-free mice. Microbes induce monounsaturated fatty acid generation by stearoyl-CoA desaturase 1 and polyunsaturated fatty acid elongation by fatty acid elongase 5, leading to significant alterations in glycerophospholipid acyl-chain profiles. A composite classification score calculated from the observed alterations in fatty acid profiles in germfree mice clearly differentiates antibiotic-treated mice from untreated controls with high sensitivity. Mechanistic investigations reveal that acetate originating from gut microbial degradation of dietary fiber serves as precursor for hepatic synthesis of C16 and C18 fatty acids and their related glycerophospholipid species that are also released into the circulation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Tandem Mass-spectrometry; Lipid-metabolism; Host Energy; Quantification; Chromatography; Fractionation; Sequences; Disease; Phospholipids; Mechanisms
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 9, Heft: 1, Seiten: , Artikelnummer: 3760 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Computational Biology (ICB)