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    Resistin down-regulates insulin receptor expression, and modulates cell viability in rodent pancreatic beta-cells.

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    Authors
    Brown, James E. P.
    Onyango, David J.
    Dunmore, Simon J.
    Issue Date
    2007
    
    Metadata
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    Abstract
    The adipokine resistin is known to induce insulin resistance in rodent tissues. Increases in adipose tissue mass are known to have a negative effect on pancreatic beta-cell function, although the mechanisms are poorly understood. This study investigated the effects of resistin on insulin secretion, insulin receptor expression and cell viability in pancreatic beta-cells. BTC-6 or BRIN-BD11 cells were treated for 24h with resistin, and insulin receptor expression, insulin secretion and cell viability were measured. Incubation with 40ng/ml resistin caused significant decreases in insulin receptor mRNA and protein expression, but did not affect insulin secretion. At low concentrations, resistin caused significant increases in cell viability. These data implicate resistin as a factor that may regulate beta-cell function/viability, and suggests a potential mechanism by which increased adiposity causes beta-cell dysfunction.
    Citation
    FEBS Letters, 581(17): 3273-3276
    Publisher
    Elsevier
    URI
    http://hdl.handle.net/2436/20394
    DOI
    10.1016/j.febslet.2007.06.031
    PubMed ID
    17597619
    Additional Links
    http://linkinghub.elsevier.com/retrieve/pii/S0014579307006680
    Type
    Journal article
    Language
    en
    ISSN
    0014-5793
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.febslet.2007.06.031
    Scopus Count
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    Research Institute in Healthcare Science

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