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Growth hormone-releaser diet attenuates cognitive dysfunction in klotho mutant mice via insulin-like growth factor-1 receptor activation in a genetic aging model

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dc.contributor.authorPark, S.J.-
dc.contributor.authorChung, Y.H.-
dc.contributor.authorLee, J.H.-
dc.contributor.authorDang, D.-K.-
dc.contributor.authorNam, Y.-
dc.contributor.authorJeong, J.H.-
dc.contributor.authorKim, Y.S.-
dc.contributor.authorNabeshima, T.-
dc.contributor.authorShin, E.-J.-
dc.contributor.authorKim, H.-C.-
dc.date.available2019-03-09T00:39:20Z-
dc.date.issued2014-
dc.identifier.issn2093-596X-
dc.identifier.issn2093-5978-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/13822-
dc.description.abstractBackground: It has been recognized that a defect in klotho gene expression accelerates the degeneration of multiple age-sensitive traits. Accumulating evidence indicates that aging is associated with declines in cognitive function and the activity of growth hormone (GH)/insulin-like growth factor-1 (IGF-1). Methods: In this study, we examined whether a GH-releaser diet could be effective in protecting against cognitive impairment in klotho mutant mice. Results: The GH-releaser diet significantly induced the expression of IGF-1 and IGF-1 receptors in the hippocampus of klotho mutant mice. Klotho mutant mice showed significant memory impairments as compared with wild-type mice. In addition, the klotho mutation significantly decreased the expression of cell survival/antiapoptotic factors, including phospho-Akt (p-Akt)/phospho- glycogen synthase kinase3β (p-GSK3β), phospho-extracellular signal-related kinase (p-ERK), and Bcl-2, but significantly increased those of cell death/proapoptotic factors, such as phospho-c-jun N-terminal kinase (p-JNK), Bax, and cleaved caspase-3 in the hippocampus. Treatment with GH-releaser diet significantly attenuated both decreases in the expression of cell survival/antiapoptotic factors and increases in the expression of cell death/proapoptotic factors in the hippocampus of klotho mutant mice. In addition, klotho mutation-induced oxidative stress was significantly attenuated by the GH-releaser diet. Consequently, a GH-releaser diet significantly improved memory function in the klotho mutant mice. GH-releaser diet-mediated actions were significantly reversed by JB-1, an IGF-1 receptor antagonist. Conclusion: The results suggest that a GH-releaser diet attenuates oxidative stress, proapoptotic changes and consequent dysfunction in klotho mutant mice by promoting IGF-1 expression and IGF-1 receptor activation. © 2014 Korean Endocrine Society.-
dc.format.extent13-
dc.language영어-
dc.language.isoENG-
dc.publisherKorean Endocrine Society-
dc.titleGrowth hormone-releaser diet attenuates cognitive dysfunction in klotho mutant mice via insulin-like growth factor-1 receptor activation in a genetic aging model-
dc.typeArticle-
dc.identifier.doi10.3803/EnM.2014.29.3.336-
dc.identifier.bibliographicCitationEndocrinology and Metabolism, v.29, no.3, pp 336 - 348-
dc.identifier.kciidART001920396-
dc.description.isOpenAccessY-
dc.identifier.scopusid2-s2.0-84930707027-
dc.citation.endPage348-
dc.citation.number3-
dc.citation.startPage336-
dc.citation.titleEndocrinology and Metabolism-
dc.citation.volume29-
dc.type.docTypeArticle-
dc.publisher.location대한민국-
dc.subject.keywordAuthorCognitive dysfunction-
dc.subject.keywordAuthorGH-releaser diet-
dc.subject.keywordAuthorKlotho gene-
dc.subject.keywordAuthorReceptor, IGF type 1-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
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