Serotonin signals through a gut-liver axis to regulate hepatic steatosis

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dc.contributor.authorChoi, Wonsukko
dc.contributor.authorNamkung, Junko
dc.contributor.authorHwang, Inseonko
dc.contributor.authorKim, Hyeongseokko
dc.contributor.authorLim, Ajinko
dc.contributor.authorPark, Hye Jungko
dc.contributor.authorLee, Hye Wonko
dc.contributor.authorHan, Kwang-Hyubko
dc.contributor.authorPark, Seongyeolko
dc.contributor.authorJeong, Ji-Seonko
dc.contributor.authorBang, Geulko
dc.contributor.authorKim, Young Hwanko
dc.contributor.authorYadav, Vijay K.ko
dc.contributor.authorKarsenty, Gerardko
dc.contributor.authorJu, Young Seokko
dc.contributor.authorChoi, Chanko
dc.contributor.authorSuh, Jae Myoungko
dc.contributor.authorPark, Jun Yongko
dc.contributor.authorPark, Sangkyuko
dc.contributor.authorKim, Hailko
dc.date.accessioned2018-12-20T05:10:21Z-
dc.date.available2018-12-20T05:10:21Z-
dc.date.created2018-12-03-
dc.date.created2018-12-03-
dc.date.created2018-12-03-
dc.date.created2018-12-03-
dc.date.issued2018-11-
dc.identifier.citationNATURE COMMUNICATIONS, v.9-
dc.identifier.issn2041-1723-
dc.identifier.urihttp://hdl.handle.net/10203/247623-
dc.description.abstractNonalcoholic fatty liver disease (NAFLD) is increasing in worldwide prevalence, closely tracking the obesity epidemic, but specific pharmaceutical treatments for NAFLD are lacking. Defining the key molecular pathways underlying the pathogenesis of NAFLD is essential for developing new drugs. Here we demonstrate that inhibition of gut-derived serotonin synthesis ameliorates hepatic steatosis through a reduction in liver serotonin receptor 2A (HTR2A) signaling. Local serotonin concentrations in the portal blood, which can directly travel to and affect the liver, are selectively increased by high-fat diet (HFD) feeding in mice. Both gut-specific Tph1 knockout mice and liver-specific Htr2a knockout mice are resistant to HFD-induced hepatic steatosis, without affecting systemic energy homeostasis. Moreover, selective HTR2A antagonist treatment prevents HFD-induced hepatic steatosis. Thus, the gut TPH1-liver HTR2A axis shows promise as a drug target to ameliorate NAFLD with minimal systemic metabolic effects.-
dc.languageEnglish-
dc.publisherNATURE PUBLISHING GROUP-
dc.titleSerotonin signals through a gut-liver axis to regulate hepatic steatosis-
dc.typeArticle-
dc.identifier.wosid000450273500011-
dc.identifier.scopusid2-s2.0-85056696823-
dc.type.rimsART-
dc.citation.volume9-
dc.citation.publicationnameNATURE COMMUNICATIONS-
dc.identifier.doi10.1038/s41467-018-07287-7-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.contributor.localauthorJu, Young Seok-
dc.contributor.localauthorSuh, Jae Myoung-
dc.contributor.localauthorKim, Hail-
dc.contributor.nonIdAuthorPark, Hye Jung-
dc.contributor.nonIdAuthorLee, Hye Won-
dc.contributor.nonIdAuthorHan, Kwang-Hyub-
dc.contributor.nonIdAuthorJeong, Ji-Seon-
dc.contributor.nonIdAuthorBang, Geul-
dc.contributor.nonIdAuthorKim, Young Hwan-
dc.contributor.nonIdAuthorYadav, Vijay K.-
dc.contributor.nonIdAuthorKarsenty, Gerard-
dc.contributor.nonIdAuthorChoi, Chan-
dc.contributor.nonIdAuthorPark, Jun Yong-
dc.description.isOpenAccessY-
dc.type.journalArticleArticle-
dc.subject.keywordPlusNF-KAPPA-B-
dc.subject.keywordPlusNONALCOHOLIC STEATOHEPATITIS-
dc.subject.keywordPlusSARPOGRELATE HYDROCHLORIDE-
dc.subject.keywordPlusPERIPHERAL SEROTONIN-
dc.subject.keywordPlusANTIPLATELET AGENT-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusTRYPTOPHAN-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusMICE-
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