1608 1908

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1-Deoxynojirimycin Isolated from a Bacillus subtilis Stimulates Adiponectin and GLUT4 Expressions in 3T3-L1 Adipocytes

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dc.contributor.author정지형-
dc.date.accessioned2014-12-18T08:50:37Z-
dc.date.available2014-12-18T08:50:37Z-
dc.date.issued2013-
dc.identifier.issn1017-7825-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/87054-
dc.description.abstractWe have demonstrated that 1-deoxynojirimycin (DNJ) isolated from Bacillus subtilis MORI could enhance the levels of adiponectin and its receptors in differentiated 3T3-L1 adipocytes, which has been shown to be effective in lowering blood glucose levels and enhancing insulin sensitivity. DNJ was not toxic to differentiated 3T3-L1 adipocytes for up to a concentration of 5 μM. In terms of expression levels of adiponectin and its receptors (AdipoR1 and AdipoR2), DNJ in concentrations as low as 0.5 μM elevated both mRNA and protein levels of adiponectin and transcript levels of AdipoR1 and AdipoR2. In addition, DNJ increased phosphorylation of 5' adenosine monophosphateactivated protein kinase (AMPK) in a statistically significant manner. Finally, treatment with DNJ resulted in increased mRNA expression of glucose transporter 4 (GLUT4), which encodes for a glucose transporter, along with a significant increase in glucose uptake into the adipocytes based on results of a 2-deoxy-D-[3H] glucose uptake assay. Our findings indicate that DNJ may greatly facilitate glucose uptake into adipose tissues by increasing the action of adiponectin via its up-regulated expression as well as its receptor genes. In addition, the glucose-lowering effects of DNJ may be achieved by an increased abundance of GLUT4 protein in the plasma membrane, as a consequence of the increased transcript levels of the GLUT4 gene and the activation of AMPK.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfJOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESH1-Deoxynojirimycin/isolation & purification-
dc.subject.MESH1-Deoxynojirimycin/pharmacology*-
dc.subject.MESH3T3-L1 Cells-
dc.subject.MESHAdipocytes/drug effects-
dc.subject.MESHAdipocytes/metabolism-
dc.subject.MESHAdiponectin/genetics*-
dc.subject.MESHAdiponectin/metabolism-
dc.subject.MESHAnimals-
dc.subject.MESHBacillus subtilis/chemistry*-
dc.subject.MESHBiological Transport/drug effects-
dc.subject.MESHGlucose/metabolism-
dc.subject.MESHGlucose Transporter Type 4/genetics*-
dc.subject.MESHGlucose Transporter Type 4/metabolism-
dc.subject.MESHInsulin/metabolism-
dc.subject.MESHMice-
dc.subject.MESHUp-Regulation/drug effects*-
dc.title1-Deoxynojirimycin Isolated from a Bacillus subtilis Stimulates Adiponectin and GLUT4 Expressions in 3T3-L1 Adipocytes-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.departmentYonsei Cardiovascular Research Institute (심혈관연구소)-
dc.contributor.googleauthorSeung-Min Lee-
dc.contributor.googleauthorHyun Ju Do-
dc.contributor.googleauthorMin-Jeong Shin-
dc.contributor.googleauthorSu-Il Seong-
dc.contributor.googleauthorKyo Yeol Hwang-
dc.contributor.googleauthorJae Yeon Lee-
dc.contributor.googleauthorOhsuk Kwon-
dc.contributor.googleauthorTaewon Jin-
dc.contributor.googleauthorJi Hyung Chung-
dc.identifier.doi10.4014/jmb.1209.09043-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03739-
dc.relation.journalcodeJ01594-
dc.identifier.eissn1738-8872-
dc.identifier.pmid23648852-
dc.subject.keyword1-Deoxynojirimycin-
dc.subject.keywordadipocytes-
dc.subject.keywordadiponectin-
dc.subject.keywordAdipoR-
dc.subject.keywordAMPK-
dc.contributor.alternativeNameChung, Ji Hyung-
dc.contributor.affiliatedAuthorChung, Ji Hyung-
dc.rights.accessRightsfree-
dc.citation.volume23-
dc.citation.number5-
dc.citation.startPage637-
dc.citation.endPage643-
dc.identifier.bibliographicCitationJOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY, Vol.23(5) : 637-643, 2013-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers

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