IL1R1 is required for celastrol's leptin-sensitization and antiobesity effects

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dc.contributor.authorFeng, Xudongko
dc.contributor.authorGuan, Dongxianko
dc.contributor.authorAuen, Thomasko
dc.contributor.authorChoi, Jae Wonko
dc.contributor.authorHernandez, Mario Andres Salazarko
dc.contributor.authorLee, Jaeminko
dc.contributor.authorChun, Hyonhoko
dc.contributor.authorFaruk, Farhanako
dc.contributor.authorKaplun, Estherko
dc.contributor.authorHerbert, Zacharyko
dc.contributor.authorCopps, Kyle D.ko
dc.contributor.authorOzcan, Umutko
dc.date.accessioned2020-03-19T02:24:53Z-
dc.date.available2020-03-19T02:24:53Z-
dc.date.created2020-03-12-
dc.date.created2020-03-12-
dc.date.issued2019-04-
dc.identifier.citationNATURE MEDICINE, v.25, no.4, pp.575 - +-
dc.identifier.issn1078-8956-
dc.identifier.urihttp://hdl.handle.net/10203/272648-
dc.description.abstractCelastrol, a pentacyclic triterpene, is the most potent antiobesity agent that has been reported thus far(1). The mechanism of celastrol's leptin-sensitizing and antiobesity effects has not yet been elucidated. In this study, we identified interleukin-1 receptor 1 (IL1R1) as a mediator of celastrol's action by using temporally resolved analysis of the hypothalamic transcriptome in celastrol-treated DIO, lean, and db/db mice. We demonstrate that IL1R1-deficient mice are completely resistant to the effects of celastrol in leptin sensitization and treatment of obesity, diabetes, and nonalcoholic steatohepatitis. Thus, we conclude that IL1R1 is a gatekeeper for celastrol's metabolic actions.-
dc.languageEnglish-
dc.publisherNATURE PUBLISHING GROUP-
dc.titleIL1R1 is required for celastrol's leptin-sensitization and antiobesity effects-
dc.typeArticle-
dc.identifier.wosid000463342800018-
dc.identifier.scopusid2-s2.0-85062600388-
dc.type.rimsART-
dc.citation.volume25-
dc.citation.issue4-
dc.citation.beginningpage575-
dc.citation.endingpage+-
dc.citation.publicationnameNATURE MEDICINE-
dc.identifier.doi10.1038/s41591-019-0358-x-
dc.contributor.localauthorChun, Hyonho-
dc.contributor.nonIdAuthorFeng, Xudong-
dc.contributor.nonIdAuthorGuan, Dongxian-
dc.contributor.nonIdAuthorAuen, Thomas-
dc.contributor.nonIdAuthorChoi, Jae Won-
dc.contributor.nonIdAuthorHernandez, Mario Andres Salazar-
dc.contributor.nonIdAuthorLee, Jaemin-
dc.contributor.nonIdAuthorFaruk, Farhana-
dc.contributor.nonIdAuthorKaplun, Esther-
dc.contributor.nonIdAuthorHerbert, Zachary-
dc.contributor.nonIdAuthorCopps, Kyle D.-
dc.contributor.nonIdAuthorOzcan, Umut-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordPlusUNFOLDED PROTEIN RESPONSE-
dc.subject.keywordPlusRECEPTOR SUPERFAMILY-
dc.subject.keywordPlusINSULIN SENSITIVITY-
dc.subject.keywordPlusENERGY-BALANCE-
dc.subject.keywordPlusOBESITY-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusRESISTANCE-
dc.subject.keywordPlusSTRESS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusANAKINRA-
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