Akkermansia muciniphila mediates negative effects of IFNγ on glucose metabolism
抄録
<jats:title>Abstract</jats:title><jats:p>Cross-talk between the gut microbiota and the host immune system regulates host metabolism, and its dysregulation can cause metabolic disease. Here, we show that the gut microbe <jats:italic>Akkermansia muciniphila</jats:italic> can mediate negative effects of IFNγ on glucose tolerance. In IFNγ-deficient mice, <jats:italic>A. muciniphila</jats:italic> is significantly increased and restoration of IFNγ levels reduces <jats:italic>A. muciniphila</jats:italic> abundance. We further show that IFNγ-knockout mice whose microbiota does not contain <jats:italic>A. muciniphila</jats:italic> do not show improvement in glucose tolerance and adding back <jats:italic>A. muciniphila</jats:italic> promoted enhanced glucose tolerance. We go on to identify Irgm1 as an IFNγ-regulated gene in the mouse ileum that controls gut <jats:italic>A. muciniphila</jats:italic> levels. <jats:italic>A. muciniphila</jats:italic> is also linked to IFNγ-regulated gene expression in the intestine and glucose parameters in humans, suggesting that this trialogue between IFNγ, <jats:italic>A. muciniphila</jats:italic> and glucose tolerance might be an evolutionally conserved mechanism regulating metabolic health in mice and humans.</jats:p>
収録刊行物
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- Nature Communications
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Nature Communications 7 (1), 2016-11-14
Springer Science and Business Media LLC