Sphingolipids produced by gut bacteria enter host metabolic pathways impacting ceramide levels

Elizabeth L. Johnson, Stacey L. Heaver, Jillian L. Waters, Benjamin I. Kim, Alexis Bretin, Andrew L. Goodman, Andrew T. Gewirtz, Tilla S. Worgall and Ruth E. Ley ()
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Elizabeth L. Johnson: Max Planck Institute for Developmental Biology
Stacey L. Heaver: Max Planck Institute for Developmental Biology
Jillian L. Waters: Max Planck Institute for Developmental Biology
Benjamin I. Kim: Columbia University
Alexis Bretin: Georgia State University
Andrew L. Goodman: Yale University School of Medicine
Andrew T. Gewirtz: Georgia State University
Tilla S. Worgall: Columbia University
Ruth E. Ley: Max Planck Institute for Developmental Biology

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: Abstract Gut microbes are linked to host metabolism, but specific mechanisms remain to be uncovered. Ceramides, a type of sphingolipid (SL), have been implicated in the development of a range of metabolic disorders from insulin resistance (IR) to hepatic steatosis. SLs are obtained from the diet and generated by de novo synthesis in mammalian tissues. Another potential, but unexplored, source of mammalian SLs is production by Bacteroidetes, the dominant phylum of the gut microbiome. Genomes of Bacteroides spp. and their relatives encode serine palmitoyltransfease (SPT), allowing them to produce SLs. Here, we explore the contribution of SL-production by gut Bacteroides to host SL homeostasis. In human cell culture, bacterial SLs are processed by host SL-metabolic pathways. In mouse models, Bacteroides-derived lipids transfer to host epithelial tissue and the hepatic portal vein. Administration of B. thetaiotaomicron to mice, but not an SPT-deficient strain, reduces de novo SL production and increases liver ceramides. These results indicate that gut-derived bacterial SLs affect host lipid metabolism.

Date: 2020
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DOI: 10.1038/s41467-020-16274-w

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