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    Pancreatic beta-Cell Membrane Fluidity and Toxicity Induced by Human Islet Amyloid Polypeptide Species

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    Author
    Pilkington, EH; Gurzov, EN; Kakinen, A; Litwak, SA; Stanley, WJ; Davis, TP; Ke, PC
    Date
    2016-02-16
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Gurzov, Esteban; Stanley, William; Pilkington, Emily
    Affiliation
    Medicine and Radiology
    Melbourne Dental School
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Pilkington, E. H., Gurzov, E. N., Kakinen, A., Litwak, S. A., Stanley, W. J., Davis, T. P. & Ke, P. C. (2016). Pancreatic beta-Cell Membrane Fluidity and Toxicity Induced by Human Islet Amyloid Polypeptide Species. SCIENTIFIC REPORTS, 6 (1), https://doi.org/10.1038/srep21274.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257333
    DOI
    10.1038/srep21274
    Abstract
    Aggregation of human islet amyloid polypeptide (hIAPP) into fibrils and plaques is associated with pancreatic β-cell loss in type 2 diabetes (T2D). However, due to the rapidness of hIAPP conversion in aqueous phase, exactly which hIAPP species is responsible for the observed toxicity and through what mechanisms remains ambiguous. In light of the importance of understanding hIAPP toxicity for T2D here we show a biophysical scheme based on the use of a lipophilic Laurdan dye for examining MIN6 cell membranes upon exposure to fresh and oligomeric hIAPP as well as mature amyloid. It has been found that all three hIAPP species, especially fresh hIAPP, enhanced membrane fluidity and caused losses in cell viability. The cell generation of reactive oxygen species (ROS), however, was the most pronounced with mature amyloid hIAPP. The correlation between changes in membrane fluidity and cell viability and their lack of correlation with ROS production suggest hIAPP toxicity is elicited through both physical and biochemical means. This study offers a new insight into β-cell toxicity induced by controlled hIAPP species, as well as new biophysical methodologies that may prove beneficial for the studies of T2D as well as neurological disorders.

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