Effect of scopoletin on lipoprotein lipase activity in 3T3-L1 adipocytes

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dc.contributor.authorYang, Jeong-Yehko
dc.contributor.authorKoo, Jeung-Hyunko
dc.contributor.authorYoon, Ha-Yongko
dc.contributor.authorLee, Ju-Hyungko
dc.contributor.authorPark, Byung-Hyunko
dc.contributor.authorKim, Jong-Sukko
dc.contributor.authorChi, Myung S.ko
dc.contributor.authorPark, Jin-Wooko
dc.date.accessioned2024-03-22T05:01:24Z-
dc.date.available2024-03-22T05:01:24Z-
dc.date.created2024-03-21-
dc.date.created2024-03-21-
dc.date.issued2007-10-
dc.identifier.citationINTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.20, no.4, pp.527 - 531-
dc.identifier.issn1107-3756-
dc.identifier.urihttp://hdl.handle.net/10203/318700-
dc.description.abstractHypertriglyceridemia is an independent risk factor of cardiovascular diseases. It is caused by the imbalance between hepatic triglyceride production and peripheral removal. Lipoprotein lipase (LPL) plays a central role in the removal of plasma triglyceride. During the screening of possible anti-dyslipidemic drugs, we observed that scopoletin (6-metboxy-7-hydroxycoumarin) significantly increased LPL activity in adipocytes. Scopoletin increased LPL activity in culture medium of 3T3-L1 adipocytes in dose- and time-dependent manners. It did not release LPL from the adipocyte membrane and, instead, increased the LPL mRNA level, suggesting transcriptional control. Scopoletin also partially reversed tumor necrosis factor-alpha induced suppression of LPL activity. These results suggest the possible action of scopoletin as a facilitator of plasma triglyceride clearance.-
dc.languageEnglish-
dc.publisherPROFESSOR D A SPANDIDOS-
dc.titleEffect of scopoletin on lipoprotein lipase activity in 3T3-L1 adipocytes-
dc.typeArticle-
dc.identifier.wosid000249797000014-
dc.type.rimsART-
dc.citation.volume20-
dc.citation.issue4-
dc.citation.beginningpage527-
dc.citation.endingpage531-
dc.citation.publicationnameINTERNATIONAL JOURNAL OF MOLECULAR MEDICINE-
dc.contributor.localauthorPark, Byung-Hyun-
dc.contributor.nonIdAuthorYang, Jeong-Yeh-
dc.contributor.nonIdAuthorKoo, Jeung-Hyun-
dc.contributor.nonIdAuthorYoon, Ha-Yong-
dc.contributor.nonIdAuthorLee, Ju-Hyung-
dc.contributor.nonIdAuthorKim, Jong-Suk-
dc.contributor.nonIdAuthorChi, Myung S.-
dc.contributor.nonIdAuthorPark, Jin-Woo-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordPlusTUMOR-NECROSIS-FACTOR-
dc.subject.keywordPlusACTIVATOR NO-1886-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusHYPERTRIGLYCERIDEMIA-
dc.subject.keywordPlusATHEROSCLEROSIS-
dc.subject.keywordPlusSECRETION-
dc.subject.keywordPlusGLYCOSYLATION-
dc.subject.keywordPlusDIMERIZATION-
dc.subject.keywordPlusCONSTITUENT-
dc.subject.keywordPlusRATS-
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