{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T19:26:36Z","timestamp":1790796396467,"version":"4.1.0"},"reference-count":51,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2015,7,2]],"date-time":"2015-07-02T00:00:00Z","timestamp":1435795200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Bio & Medical Technology Development Program","award":["NRF-2012M3A9B2027975"],"award-info":[{"award-number":["NRF-2012M3A9B2027975"]}]},{"name":"Basic Science Research Program","award":["2013012280"],"award-info":[{"award-number":["2013012280"]}]},{"name":"Medical Research Center Program","award":["2008-0062279"],"award-info":[{"award-number":["2008-0062279"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Nutrition Food Res"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:sec><jats:title>Scope<\/jats:title><jats:p>In this study, we focus on the effects of n\u20103 polyunsaturated fatty acids (PUFAs) on tunicamycin\u2010, streptozotocin\u2010, or high fat diet (HFD)\u2010induced \u03b2\u2010cell damage and dysfunction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and methods<\/jats:title><jats:p>Pretreatment with n\u20103 PUFAs protected RINm5F cells and mouse islets against tunicamycin\u2010induced \u03b2\u2010cell damage through suppression of ER stress and apoptosis induction. This protective effect of n\u20103 PUFAs on \u03b2\u2010cells was further demonstrated by the normalization of insulin secretion in response to glucose in tunicamycin\u2010treated islets. In multiple low\u2010dose streptozotocin\u2010induced diabetes models, <jats:italic>fat\u20101<\/jats:italic> mice, which endogenously synthesize n\u20103 PUFAs from n\u20106 PUFAs, were fully resistant to the development of diabetes, with normal islet morphology, high insulin immunoreactivity, and decreased apoptotic cells. In HFD\u2010induced diabetes models, <jats:italic>fat\u20101<\/jats:italic> mice also exhibited improved glucose tolerance and functional \u03b2\u2010cell mass. In both diabetes models, we observed an attenuation of ER stress in <jats:italic>fat\u20101<\/jats:italic> mice. Interestingly, n\u20103 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element\u2010binding protein\u20101 (SREBP\u20101) and C\/EBP\u03b2, induced by tunicamycin or HFD, suggesting that n\u20103 PUFAs suppress ER stress via modulation of SREBP\u20101 and C\/EBP\u03b2.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Together, these results suggest that n\u20103 PUFAs block ER stress, thus protecting \u03b2 cells against diabetogenic insult; therefore, dietary supplementation of n\u20103 PUFAs has therapeutic potential for the preservation of functional \u03b2\u2010cell mass.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mnfr.201500299","type":"journal-article","created":{"date-parts":[[2015,6,16]],"date-time":"2015-06-16T03:51:10Z","timestamp":1434426670000},"page":"1791-1802","source":"Crossref","is-referenced-by-count":26,"title":["n\u20103 Polyunsaturated fatty acids protect against pancreatic \u03b2\u2010cell 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