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Gut microbiota modifies bile acid pool to generate CBAs and then CBAs returned to liver to regulate hepatic genes, fatty liver, and non\u2010alcoholic fatty liver disease (NAFLD). However, it is not yet known how the gut microbiota was modified under the environment of inflammatory bowel disease (IBD). Here, we revealed that aberrant intestinal sphingosine kinases (SphKs), a major risk factor of IBD, modified gut microbiota by increasing the proportions of\n                    <jats:italic>Firmicutes<\/jats:italic>\n                    and\n                    <jats:italic>Verrucomicrobia<\/jats:italic>\n                    , which were associated with the increase in CBAs. When exposed to a high\u2010fat diet (HFD), sphingosine kinases 2\u00a0knockout (SphK2KO) mice developed more severity of intestinal inflammation and hepatic steatosis than their wild\u2010type (WT) littermates. Due to knockdown of nuclear SphK2, Sphk2KO mice exhibited an increase in sphingosine kinases 1 (SphK1) and sphingosine\u20101\u2010phosphate (S1P) in intestinal epithelial cells. Therefore, the microbiota was modified in the environment of the SphK1\/S1P\u2010induced IBD. 16S rDNA amplicon sequencing of cecal contents indicated an increase of\n                    <jats:italic>Firmicutes<\/jats:italic>\n                    and\n                    <jats:italic>Verrucomicrobia<\/jats:italic>\n                    . Ultra\u2010performance liquid chromatography coupled to tandem mass spectrometry (UPLC\u2010MS\/MS) measured an increase in CBAs, including taurocholic acid (TCA), taurodeoxycholic acid (TDCA), and glycocholic acid (GCA), in cecal contents and liver tissues of Sphk2KO mice. These CBAs accumulated in the liver promoted hepatic steatosis through downregulating the acetylation of H3K9, H3K14, H3K18 and H3K27 due to the CBAs\u2010S1PR2\u2010nuclear SphK2\u2010S1P signaling pathway was blocked in HFD\u2010SphK2KO mice. In summary, intestinal aberrant sphingolipid metabolism developed hepatic steatosis through the increase in CBAs associated with an increase in\n                    <jats:italic>Firmicutes<\/jats:italic>\n                    and\n                    <jats:italic>Verrucomicrobia<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1096\/fj.202200148rr","type":"journal-article","created":{"date-parts":[[2022,7,6]],"date-time":"2022-07-06T10:39:59Z","timestamp":1657103999000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Intestinal aberrant sphingolipid metabolism shaped\u2010gut microbiome and bile acids metabolome in the development of hepatic steatosis"],"prefix":"10.1096","volume":"36","author":[{"given":"Rong\u2010Rong","family":"Miao","sequence":"first","affiliation":[{"name":"Department of Pharmacology School of Basic Medical Sciences Capital Medical University  Beijing 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