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DC Field | Value | Language |
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dc.citation.endPage | 803 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 793 | - |
dc.citation.title | ENDOCRINOLOGY | - |
dc.citation.volume | 152 | - |
dc.contributor.author | Lee, Joo-Won | - |
dc.contributor.author | Choi, A. Hyun | - |
dc.contributor.author | Ham, Mira | - |
dc.contributor.author | Kim, Ji-Won | - |
dc.contributor.author | Choe, Sung Sik | - |
dc.contributor.author | Park, Jiyoung | - |
dc.contributor.author | Lee, Gha Young | - |
dc.contributor.author | Yoon, Kun-Ho | - |
dc.contributor.author | Kim, Jae Bum | - |
dc.date.accessioned | 2023-12-22T06:15:50Z | - |
dc.date.available | 2023-12-22T06:15:50Z | - |
dc.date.created | 2014-10-13 | - |
dc.date.issued | 2011-03 | - |
dc.description.abstract | Increased reactive oxygen species (ROS) induce pancreatic β-cell dysfunction during progressive type 2 diabetes. Glucose-6-phosphate dehydrogenase (G6PD) is a reduced nicotinamide adenine dinucleotide phosphate-producing enzyme that plays a key role in cellular reduction/oxidation regulation. We have investigated whether variations in G6PD contribute to β-cell dysfunction through regulation of ROS accumulation and β-cell gene expression. When the level of G6PD expression in pancreatic islets was examined in several diabetic animal models, such as db/db mice and OLEFT rats, G6PD expression was evidently up-regulated in pancreatic islets in diabetic animals. To investigate the effect of G6PD on β-cell dysfunction, we assessed the levels of cellular ROS, glucose-stimulated insulin secretion and β-cell apoptosis in G6PD-overexpressing pancreatic β-cells. In INS-1 cells, G6PD overexpression augmented ROS accumulation associated with increased expression of prooxidative enzymes, such as inducible nitric oxide synthase and reduced nicotin-amide adenine dinucleotide phosphate oxidase. G6PD up-regulation also caused decrease in glucose-stimulated insulin secretion in INS-1 cells and primary pancreatic islets. Moreover, elevated G6PD expression led to β-cell apoptosis, concomitant with the increase in proapoptotic gene expression. On the contrary, suppression of G6PD with small interference RNA attenuated palmitate-induced β-cell apoptosis. Together, these data suggest that up-regulation of G6PD in pancreatic β-cells would induce β-cell dysregulation through ROS accumulation in the development of type 2 diabetes. | - |
dc.identifier.bibliographicCitation | ENDOCRINOLOGY, v.152, no.3, pp.793 - 803 | - |
dc.identifier.doi | 10.1210/en.2010-0606 | - |
dc.identifier.issn | 0013-7227 | - |
dc.identifier.scopusid | 2-s2.0-79951868193 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/7166 | - |
dc.identifier.url | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=79951868193 | - |
dc.identifier.wosid | 000287520900007 | - |
dc.language | 영어 | - |
dc.publisher | ENDOCRINE SOC | - |
dc.title | G6PD Up-Regulation Promotes Pancreatic beta-Cell Dysfunction | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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