DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wang, Jie | ko |
dc.contributor.author | Song, Mi-Young | ko |
dc.contributor.author | Bae, Ui-Jin | ko |
dc.contributor.author | Lim, Jung Min | ko |
dc.contributor.author | Kwon, Keun Sang | ko |
dc.contributor.author | Park, Byung-Hyun | ko |
dc.date.accessioned | 2024-03-25T01:00:10Z | - |
dc.date.available | 2024-03-25T01:00:10Z | - |
dc.date.created | 2024-03-21 | - |
dc.date.created | 2024-03-21 | - |
dc.date.created | 2024-03-21 | - |
dc.date.issued | 2015-09 | - |
dc.identifier.citation | MOLECULAR NUTRITION FOOD RESEARCH, v.59, no.9, pp.1791 - 1802 | - |
dc.identifier.issn | 1613-4125 | - |
dc.identifier.uri | http://hdl.handle.net/10203/318822 | - |
dc.description.abstract | Scope: In this study, we focus on the effects of n-3 polyunsaturated fatty acids (PUFAs) on tunicamycin-, streptozotocin-, or high fat diet (HFD)-induced beta-cell damage and dysfunction. Materials and methods: Pretreatment with n-3 PUFAs protected RINm5F cells and mouse islets against tunicamycin- induced beta-cell damage through suppression of ER stress and apoptosis induction. This protective effect of n-3 PUFAs on beta-cells was further demonstrated by the normalization of insulin secretion in response to glucose in tunicamycin- treated islets. In multiple low-dose streptozotocin- induced diabetes models, fat-1 mice, which endogenously synthesize n-3 PUFAs from n-6 PUFAs, were fully resistant to the development of diabetes, with normal islet morphology, high insulin immunoreactivity, and decreased apoptotic cells. In HFD-induced diabetes models, fat-1 mice also exhibited improved glucose tolerance and functional beta-cell mass. In both diabetes models, we observed an attenuation of ER stress in fat-1 mice. Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBP beta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBP beta. Conclusion: Together, these results suggest that n-3 PUFAs block ER stress, thus protecting beta cells against diabetogenic insult; therefore, dietary supplementation of n-3 PUFAs has therapeutic potential for the preservation of functional beta-cell mass. | - |
dc.language | English | - |
dc.publisher | WILEY | - |
dc.title | n-3 Polyunsaturated fatty acids protect against pancreatic β-cell damage due to ER stress and prevent diabetes development | - |
dc.type | Article | - |
dc.identifier.wosid | 000362551400014 | - |
dc.identifier.scopusid | 2-s2.0-84942837113 | - |
dc.type.rims | ART | - |
dc.citation.volume | 59 | - |
dc.citation.issue | 9 | - |
dc.citation.beginningpage | 1791 | - |
dc.citation.endingpage | 1802 | - |
dc.citation.publicationname | MOLECULAR NUTRITION FOOD RESEARCH | - |
dc.identifier.doi | 10.1002/mnfr.201500299 | - |
dc.contributor.localauthor | Park, Byung-Hyun | - |
dc.contributor.nonIdAuthor | Wang, Jie | - |
dc.contributor.nonIdAuthor | Song, Mi-Young | - |
dc.contributor.nonIdAuthor | Bae, Ui-Jin | - |
dc.contributor.nonIdAuthor | Lim, Jung Min | - |
dc.contributor.nonIdAuthor | Kwon, Keun Sang | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.subject.keywordAuthor | ER stress | - |
dc.subject.keywordAuthor | High-fat diet | - |
dc.subject.keywordAuthor | n-3 PUFAs | - |
dc.subject.keywordAuthor | Streptozotocin | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | TRANSGENIC MICE | - |
dc.subject.keywordPlus | INSULIN SENSITIVITY | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | KAPPA-B | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | SREBP-1C | - |
dc.subject.keywordPlus | ISLETS | - |
dc.subject.keywordPlus | OMEGA-3-FATTY-ACIDS | - |
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