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    High pancreatic n-3 fatty acids prevent STZ-induced diabetes in fat-1 mice: inflammatory pathway inhibition

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    Publication date
    2011
    Author
    Nicolaou, Anna
    Bellenger, J.
    Bellenger, S.
    Bataille, A.
    Massey, Karen A.
    Rialland, M.
    Tessier, C.
    Kang, J.X.
    Narce, M.
    Keyword
    Lipid Mediators
    Eicosanoids
    N-3 Fatty Acids
    Lipidomics
    Peer-Reviewed
    Yes
    
    Metadata
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    Abstract
    Because of confounding factors, the effects of dietary n-3 polyunsaturated fatty acids (PUFA) on type 1 diabetes remain to be clarified. We therefore evaluated whether fat-1 transgenic mice, a well-controlled experimental model endogenously synthesizing n-3 PUFA, were protected against streptozotocin (STZ)-induced diabetes. We then aimed to elucidate the in vivo response at the pancreatic level. Beta-Cell destruction was produced by multiple low-doses STZ (MLD-STZ). Blood glucose level, plasma insulin level, and plasma lipid analysis were then performed. Pancreatic mRNA expression of cytokines, the monocyte chemoattractant protein, and GLUT2 were evaluated as well as pancreas nuclear factor (NF)-kB p65 and inhibitor of kB (IkB) protein expression. Insulin and cleaved caspase-3 immunostaining and lipidomic analysis were performed in the pancreas. STZ-induced fat-1 mice did not develop hyperglycemia compared with wild-type mice, and Beta-cell destruction was prevented as evidenced by lack of histological pancreatic damage or reduced insulin level. The prevention of Beta-cell destruction was associated with no proinflammatory cytokine induction (tumor necrosis factor-alpha, interleukin-1Beta, inducible nitric oxide synthase) in the pancreas, a decreased NF-kB, and increased IkB pancreatic protein expression. In the fat-1-treated mice, proinflammatory arachidonic-derived mediators as prostaglandin E2 and 12-hydroxyeicosatetraenoic acid were decreased and the anti-inflammatory lipoxin A4 was detected. Moreover, the 18-hydroxyeicosapentaenoic acid, precursor of the anti-inflammatory resolvin E1, was highly increased. Collectively, these findings indicate that fat-1 mice were protected against MLD-STZ-induced diabetes and pointed out for the first time in vivo the beneficial effects of n-3 PUFA at the pancreatic level, on each step of the development of the pathology-inflammation, Beta-cell damage-through cytokine response and lipid mediator production.
    URI
    http://hdl.handle.net/10454/5231
    Version
    No full-text available in the repository
    Citation
    Nicolaou, A. (2011). High pancreatic n-3 fatty acids prevent STZ-induced diabetes in fat-1 mice: inflammatory pathway inhibition. Diabetes. Vol. 60, No. 4. pp. 1090-1099.
    Link to publisher’s version
    http://dx.doi.org/10.2337/db10-0901
    Type
    Article
    Collections
    Life Sciences Publications

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