3-Caffeoyl, 4-dihydrocaffeoylquinic acid from Salicornia herbacea attenuates high glucose-induced hepatic lipogenesis in human HepG2 cells through activation of the liver kinase B1 and silent information regulator T1/AMPK-dependent pathway

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dc.contributor.authorY P Hwang-
dc.contributor.authorH G Kim-
dc.contributor.authorJ H Choi-
dc.contributor.authorM T Do-
dc.contributor.authorT P Tran-
dc.contributor.authorHyo Kon Chun-
dc.contributor.authorY C Chung-
dc.contributor.authorT C Jeong-
dc.contributor.authorH G Jeong-
dc.date.accessioned2017-04-19T09:38:32Z-
dc.date.available2017-04-19T09:38:32Z-
dc.date.issued2013-
dc.identifier.issn1613-4125-
dc.identifier.uri10.1002/mnfr.201200529ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11269-
dc.description.abstractScope: Increasing evidence indicates that polyphenols may protect against metabolic disease through activating AMP-activated protein kinase (AMPK). The aims of our study were to provide new data on the molecular mechanism(s) underlying the role of the phenolic compound, 3-caffeoyl, 4-dihydrocaffeoylquinic acid (CDCQ) from Salicornia herbacea, in the prevention of high glucose-induced lipogenesis in human HepG2 cells. Methods and results: Nile red staining assays were used to demonstrate lipid accumulation in the cells. Expression of sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) gene at the levels of promoter activity, mRNA, and protein was demonstrated using transient transfection assays, quantitative RT-PCR, and Western blot analyses, respectively. We found that CDCQ suppressed high glucose-induced lipid accumulation in HepG2 cells. CDCQ strongly inhibited high glucose-induced FAS expression by modulating SREBP-1c activation. Moreover, the use of both a specific inhibitor and liver kinase B1 (LKB1)-siRNA transfected HepG2 cells showed that CDCQ activated AMPK via silent information regulator T1 (SIRT1) or LKB1 in HepG2 cells. Conclusion: These results indicate that CDCQ prevented lipid accumulation by blocking the expression of SREBP-1c and FAS through LKB1/SIRT1 and AMPK activation in HepG2 cells, suggesting that CDCQ plays a potential role in the prevention of lipogenesis by AMPK activation.-
dc.publisherWiley-
dc.title3-Caffeoyl, 4-dihydrocaffeoylquinic acid from Salicornia herbacea attenuates high glucose-induced hepatic lipogenesis in human HepG2 cells through activation of the liver kinase B1 and silent information regulator T1/AMPK-dependent pathway-
dc.title.alternative3-Caffeoyl, 4-dihydrocaffeoylquinic acid from Salicornia herbacea attenuates high glucose-induced hepatic lipogenesis in human HepG2 cells through activation of the liver kinase B1 and silent information regulator T1/AMPK-dependent pathway-
dc.typeArticle-
dc.citation.titleMolecular Nutrition & Food Research-
dc.citation.number3-
dc.citation.endPage482-
dc.citation.startPage471-
dc.citation.volume57-
dc.contributor.affiliatedAuthorHyo Kon Chun-
dc.contributor.alternativeName황용필-
dc.contributor.alternativeName김형균-
dc.contributor.alternativeName최재호-
dc.contributor.alternativeNameDo-
dc.contributor.alternativeNameTran-
dc.contributor.alternativeName전효곤-
dc.contributor.alternativeName정영철-
dc.contributor.alternativeName정태천-
dc.contributor.alternativeName정혜광-
dc.identifier.bibliographicCitationMolecular Nutrition & Food Research, vol. 57, no. 3, pp. 471-482-
dc.identifier.doi10.1002/mnfr.201200529-
dc.subject.keyword3-Caffeoyl, 4-dihydrocaffeoylquinic acid-
dc.subject.keywordAMPK-
dc.subject.keywordHigh glucose-
dc.subject.keywordLipogenesis-
dc.subject.keywordLKB1-
dc.subject.local3-Caffeoyl, 4-dihydrocaffeoylquinic acid-
dc.subject.local3-caffeoyl-4-dihydrocaffeoyl quinic acid-
dc.subject.localAMPK-
dc.subject.localHigh glucose-
dc.subject.locallipogenesis-
dc.subject.localLipogenesis-
dc.subject.localLKB1-
dc.description.journalClassY-
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Division of Bio Technology Innovation > SME Support Center > 1. Journal Articles
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