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Cited 19 times in

Glycated Albumin Causes Pancreatic β-Cells Dysfunction Through Autophagy Dysfunction

DC Field Value Language
dc.contributor.author강은석-
dc.contributor.author송선옥-
dc.contributor.author송영미-
dc.contributor.author이병완-
dc.contributor.author이현철-
dc.contributor.author차봉수-
dc.date.accessioned2014-12-18T09:11:33Z-
dc.date.available2014-12-18T09:11:33Z-
dc.date.issued2013-
dc.identifier.issn0013-7227-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/87705-
dc.description.abstractGrowing evidence suggests that advanced glycation end-products (AGEs) are cytotoxic to pancreatic β-cells. The aims of this study were to investigate whether glycated albumin (GA), an early precursor of AGEs, would induce dysfunction in pancreatic β-cells and to determine which kinds of cellular mechanisms are activated in GA-induced β-cell apoptosis. Decreased viability and increased apoptosis were induced in INS-1 cells treated with 2.5 mg/mL GA under 16.7mM high-glucose conditions. Insulin content and glucose-stimulated secretion from isolated rat islets were reduced in 2.5 mg/mL GA-treated cells. In response to 2.5 mg/mL GA in INS-1 cells, autophagy induction and flux decreased as assessed by green fluorescent protein-microtubule-associated protein 1 light chain 3 dots, microtubule-associated protein 1 light chain 3-II conversion, and SQSTM1/p62 in the presence and absence of bafilomycin A1. Accumulated SQSTM1/p62 through deficient autophagy activated the nuclear factor-κB (p65)-inducible nitric oxide synthase-caspase-3 cascade, which was restored by treatment with small interfering RNA against p62. Small interfering RNA treatment against autophagy-related protein 5 significantly inhibited the autophagy machinery resulting in a significant increase in iNOS-cleaved caspase-3 expression. Treatment with 500μM 4-phenyl butyric acid significantly alleviated the expression of endoplasmic reticulum stress markers and iNOS in parallel with upregulated autophagy induction. However, in the presence of bafilomycin A1, the decreased viability of INS-1 cells was not recovered. Glycated albumin, an early precursor of AGE, caused pancreatic β-cell death by inhibiting autophagy induction and flux, resulting in nuclear factor-κB (p65)-iNOS-caspase-3 cascade activation as well as by increasing susceptibility to endoplasmic reticulum stress and oxidative stress.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfENDOCRINOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleGlycated Albumin Causes Pancreatic β-Cells Dysfunction Through Autophagy Dysfunction-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentYonsei Biomedical Research Center (연세의생명연구원)-
dc.contributor.googleauthorYoung Mi Song-
dc.contributor.googleauthorSun Ok Song-
dc.contributor.googleauthorYoung-Hye You-
dc.contributor.googleauthorKun-Ho Yoon-
dc.contributor.googleauthorEun Seok Kang-
dc.contributor.googleauthorBong Soo Cha-
dc.contributor.googleauthorHyun Chul Lee-
dc.contributor.googleauthorJi-Won Kim-
dc.contributor.googleauthorByung-Wan Lee-
dc.identifier.doi10.1210/en.2013-1031-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00068-
dc.contributor.localIdA02029-
dc.contributor.localIdA02039-
dc.contributor.localIdA02796-
dc.contributor.localIdA03301-
dc.contributor.localIdA03996-
dc.relation.journalcodeJ00772-
dc.identifier.eissn1945-7170-
dc.identifier.urlhttp://press.endocrine.org/doi/abs/10.1210/en.2013-1031?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed&-
dc.contributor.alternativeNameKang, Eun Seok-
dc.contributor.alternativeNameSong, Sun Ok-
dc.contributor.alternativeNameSong, Young Mi-
dc.contributor.alternativeNameLee, Byung Wan-
dc.contributor.alternativeNameLee, Hyun Chul-
dc.contributor.alternativeNameCha, Bong Soo-
dc.contributor.affiliatedAuthorKang, Eun Seok-
dc.contributor.affiliatedAuthorSong, Sun Ok-
dc.contributor.affiliatedAuthorSong, Young Mi-
dc.contributor.affiliatedAuthorLee, Byung Wan-
dc.contributor.affiliatedAuthorLee, Hyun Chul-
dc.contributor.affiliatedAuthorCha, Bong Soo-
dc.rights.accessRightsnot free-
dc.citation.volume154-
dc.citation.number8-
dc.citation.startPage2626-
dc.citation.endPage2639-
dc.identifier.bibliographicCitationENDOCRINOLOGY, Vol.154(8) : 2626-2639, 2013-
dc.identifier.rimsid32221-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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