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Macroautophagy in homeostasis of pancreatic β-cell
DC Field | Value | Language |
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dc.contributor.author | Jung, Hye Seung | - |
dc.contributor.author | Lee, Myung-Shik | - |
dc.date.accessioned | 2012-06-26T00:06:07Z | - |
dc.date.available | 2012-06-26T00:06:07Z | - |
dc.date.issued | 2009-02-16 | - |
dc.identifier.citation | AUTOPHAGY; Vol.5 2; 241-243 | ko_KR |
dc.identifier.issn | 1554-8627 | - |
dc.identifier.uri | https://hdl.handle.net/10371/77406 | - |
dc.description.abstract | Diabetes mellitus is characterized by decreased insulin secretion and action. Decreased insulin secretion results from a reduction in pancreatic beta-cell mass and function. Apoptosis, oxidative stress, mitochondrial dysfunction, and ER stress responses including JNK activation have been suggested as mechanisms of the changes of pancreatic beta-cells in type 2 diabetes, however, the underlying causes were not clearly elucidated. Autophagy is an intracellular process that plays a crucial role in cellular homeostasis through degradation and recycling of organelles constitutively or in response to the environmental condition. We studied the role of autophagy in pancreatic beta-cells using mice with beta-cell-specific deletion of the Atg7 (autophagy-related 7) gene. Atg7-mutant mice showed increased apoptosis and decreased proliferation of beta-cells with resultant reduction in beta-cell mass. Pancreatic insulin content was decreased due to the decreased beta-cell mass and reduced number of insulin granules. Morphological analysis of beta-cells revealed accumulation of ubiquitinated proteins, swollen mitochondria, and distended ER. Insulin secretary function ex vivo was also impaired. As a result, autophagy-deficient mice showed hypoinsulinemia and hyperglycemia. These results suggest that autophagy is necessary to maintain structure, mass and function of pancreatic beta-cells. Here we discuss the significance of autophagy in pancreatic beta-cells with its potential relevance to the development of diabetes. | ko_KR |
dc.description.sponsorship | This work was supported by a Nano/Bio Science Program Grant
(2004-00716), and by the 21C Frontier Functional Proteomics Project of the Korean Ministry of Science & Technology (FPR08B1- 210). | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | LANDES BIOSCIENCE | ko_KR |
dc.subject | autophagy | ko_KR |
dc.subject | mitochondria | ko_KR |
dc.subject | endoplasmic reticulum | ko_KR |
dc.subject | diabetes | ko_KR |
dc.subject | pancreatic beta-cell | ko_KR |
dc.title | Macroautophagy in homeostasis of pancreatic β-cell | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 정혜승 | - |
dc.contributor.AlternativeAuthor | 이명식 | - |
dc.citation.journaltitle | AUTOPHAGY | - |
dc.description.citedreference | Jung HS, 2008, CELL METAB, V8, P318, DOI 10.1016/j.cmet.2008.08.013 | - |
dc.description.citedreference | Ebato C, 2008, CELL METAB, V8, P325, DOI 10.1016/j.cmet.2008.08.009 | - |
dc.description.citedreference | Tavernarakis N, 2008, AUTOPHAGY, V4, P870 | - |
dc.description.citedreference | Song BB, 2008, J CLIN INVEST, V118, P3378, DOI 10.1172/JCI34587 | - |
dc.description.citedreference | Ichimura Y, 2008, J BIOL CHEM, V283, P22847, DOI 10.1074/jbc.M802182200 | - |
dc.description.citedreference | Levine B, 2008, CELL, V132, P27, DOI 10.1016/j.cell.2007.12.018 | - |
dc.description.citedreference | GOZUACIK D, 2008, CELL DEATH IN PRESS | - |
dc.description.citedreference | CHOI SE, 2008, ENDOCRINOLO IN PRESS | - |
dc.description.citedreference | HANSEN M, 2008, PLOS GENET, V4, P1 | - |
dc.description.citedreference | Komatsu M, 2007, CELL, V131, P1149, DOI 10.1016/j.cell.2007.10.035 | - |
dc.description.citedreference | Uchizono Y, 2007, DIABETES OBES METAB, V9, P56, DOI 10.1111/j.1463-1326.2007.00774.x | - |
dc.description.citedreference | Marsh BJ, 2007, MOL ENDOCRINOL, V21, P2255, DOI 10.1210/me.2007-0077 | - |
dc.description.citedreference | Nakai A, 2007, NAT MED, V13, P619, DOI 10.1038/nm1574 | - |
dc.description.citedreference | Bernales S, 2007, AUTOPHAGY, V3, P285 | - |
dc.description.citedreference | Laybutt DR, 2007, DIABETOLOGIA, V50, P752, DOI 10.1007/s00125-006-0590-z | - |
dc.description.citedreference | Kaniuk NA, 2007, DIABETES, V56, P930, DOI 10.2337/db06-1160 | - |
dc.description.citedreference | Liang JY, 2007, NAT CELL BIOL, V9, P218, DOI 10.1038/ncb1537 | - |
dc.description.citedreference | CAVALLINI G, 2007, AUTOPHAGY, V3, P21 | - |
dc.description.citedreference | Ogata M, 2006, MOL CELL BIOL, V26, P9220, DOI 10.1128/MCB.01453-06 | - |
dc.description.citedreference | Karaskov E, 2006, ENDOCRINOLOGY, V147, P3398, DOI 10.1210/en.2005-1494 | - |
dc.description.citedreference | Komatsu M, 2006, NATURE, V441, P880, DOI 10.1038/nature04723 | - |
dc.description.citedreference | Hara T, 2006, NATURE, V441, P885, DOI 10.1038/nature04724 | - |
dc.description.citedreference | Wu J, 2006, CELL DEATH DIFFER, V13, P374, DOI 10.1038/sj.cdd.4401840 | - |
dc.description.citedreference | Rodriguez-Enriquez S, 2006, AUTOPHAGY, V2, P39 | - |
dc.description.citedreference | Bjorkoy G, 2005, J CELL BIOL, V171, P603, DOI 10.1083/jcb.200507002 | - |
dc.description.citedreference | Ozcan U, 2004, SCIENCE, V306, P457 | - |
dc.description.citedreference | Petersen KF, 2003, SCIENCE, V300, P1140 | - |
dc.description.citedreference | Harding HP, 2001, MOL CELL, V7, P1153 | - |
dc.description.citedreference | Maechler P, 1999, NATURE, V402, P685 | - |
dc.description.tc | 3 | - |
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