Publisher： John Wiley & Sons Inc
E-ISSN： 1613-4133|59|9|1791-1802
ISSN： 1613-4125
Source： MOLECULAR NUTRITION & FOOD RESEARCH, Vol.59, Iss.9, 2015-09, pp. : 1791-1802
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Abstract
ScopeIn this study, we focus on the effects of n‐3 polyunsaturated fatty acids (PUFAs) on tunicamycin‐, streptozotocin‐, or high fat diet (HFD)‐induced β‐cell damage and dysfunction.Materials and methodsPretreatment with n‐3 PUFAs protected RINm5F cells and mouse islets against tunicamycin‐induced β‐cell damage through suppression of ER stress and apoptosis induction. This protective effect of n‐3 PUFAs on β‐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 β‐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/EBPβ, induced by tunicamycin or HFD, suggesting that n‐3 PUFAs suppress ER stress via modulation of SREBP‐1 and C/EBPβ.ConclusionTogether, these results suggest that n‐3 PUFAs block ER stress, thus protecting β cells against diabetogenic insult; therefore, dietary supplementation of n‐3 PUFAs has therapeutic potential for the preservation of functional β‐cell mass.
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