Resistin down-regulates insulin receptor expression, and modulates cell viability in rodent pancreatic beta-cells.
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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): 3273-3276Publisher
ElsevierPubMed ID
17597619Additional Links
http://linkinghub.elsevier.com/retrieve/pii/S0014579307006680Type
Journal articleLanguage
enISSN
0014-5793ae974a485f413a2113503eed53cd6c53
10.1016/j.febslet.2007.06.031
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