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Regulation of Adiponectin Receptor 2 Expression via PPAR-alpha in NIT-1 Cells

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dc.contributor.authorJung, Tae Woo-
dc.contributor.authorLee, Myung Won-
dc.contributor.authorLee, Yong Jik-
dc.contributor.authorKim, Seon Mee-
dc.contributor.authorLee, Kyoung Tae-
dc.contributor.authorWhang, Wan Kyunn-
dc.contributor.authorCheon, Hwan Ju-
dc.contributor.authorJeong, Yeon Taek-
dc.contributor.authorChung, Kun Wook-
dc.contributor.authorCho, Jae Min-
dc.contributor.authorKim, Do Hoon-
dc.contributor.authorJung, Tae Woo-
dc.date.accessioned2021-09-08T16:31:24Z-
dc.date.available2021-09-08T16:31:24Z-
dc.date.created2021-06-10-
dc.date.issued2009-06-
dc.identifier.issn0918-8959-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/119930-
dc.description.abstractAdiponectin receptors mediate the antidiabetic effects of adiponectin. Although suggested to be mainly expressed in muscle, liver, and adipocyte cells, the expression of adiponectin receptors in beta cells is unclear. Given the primary involvement of this cell type in diabetes mellitus, we presently examined the expression level of adiponectin receptor 2 (AdiR2) in beta cells. Expression was significantly increased under acute hyperlipidemic conditions but impaired under chronic conditions. The impaired AdiR2 expression may play a role in worsened beta cell function. Clofibrate, an agonist of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) delayed the palmitate-induced impairment of AdiR2 expression and PPAR-alpha; this delay was abolished by PPAR-alpha targeted small interfering RNA. The results suggest that AdiR2 expression is regulated by palmitate via PPAR-alpha.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherJAPAN ENDOCRINE SOC-
dc.subjectACTIVATED PROTEIN-KINASE-
dc.subjectINSULIN-SECRETION-
dc.subjectRESISTANCE-
dc.subjectPREVENTS-
dc.subjectREVERSES-
dc.subjectSTATE-
dc.subjectRATS-
dc.titleRegulation of Adiponectin Receptor 2 Expression via PPAR-alpha in NIT-1 Cells-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Seon Mee-
dc.identifier.doi10.1507/endocrj.K08E-354-
dc.identifier.scopusid2-s2.0-67650496962-
dc.identifier.wosid000267689100007-
dc.identifier.bibliographicCitationENDOCRINE JOURNAL, v.56, no.3, pp.377 - 382-
dc.relation.isPartOfENDOCRINE JOURNAL-
dc.citation.titleENDOCRINE JOURNAL-
dc.citation.volume56-
dc.citation.number3-
dc.citation.startPage377-
dc.citation.endPage382-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaEndocrinology & Metabolism-
dc.relation.journalWebOfScienceCategoryEndocrinology & Metabolism-
dc.subject.keywordPlusACTIVATED PROTEIN-KINASE-
dc.subject.keywordPlusINSULIN-SECRETION-
dc.subject.keywordPlusRESISTANCE-
dc.subject.keywordPlusPREVENTS-
dc.subject.keywordPlusREVERSES-
dc.subject.keywordPlusSTATE-
dc.subject.keywordPlusRATS-
dc.subject.keywordAuthorAdiponectin receptor 2-
dc.subject.keywordAuthorperoxisome proliferator-activated receptor-alpha-
dc.subject.keywordAuthorbeta cells-
dc.subject.keywordAuthorClofibrate-
dc.subject.keywordAuthorpalmitate-
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