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Treatment of NOD mice with an IGF-I/IGFBP3 complex protects against type 1 diabetes



Treatment of NOD mice with an IGF-I/IGFBP3 complex protects against type 1 diabetes



FASEB Journal 16(5): A1046, March 22



Type 1 diabetes (T1D) results from the T cell-mediated destruction of islet beta cells. Cytokine-induced apoptosis is a major route of islet beta cell death in the pathogenesis of T1D. We investigated whether treatment of NOD mice with an IGF-I/IGFBP3 complex (SomatoKineTM, Celtrix) (SK) protects against T1D. Female NOD mice (4-5 wk-old) were injected s.c. with SK (5-50 mug/day or every other day) for 4 wks. At 35 wk of age, 20% of SK treated (20 mug/day) and 100% of PBS treated control mice were diabetic. Insulitis scores and numbers of apoptotic cells in the islets were significantly reduced in mice treated with SK for 4 wk compared to control mice. However, the intra-pancreatic expression of IFN-gamma, IL-4, MIP-1alpha and MIP-beta did not change. T cell tolerance to islet beta cells was not induced with SK treatment in adoptive transfer studies. IGF-I was found to upregulate Bcl-2 and Bcl-XL and reduce Bad and Bax expression in NOD islets and insulinsoma cells. Activation of PI-3K induced by IGF-I was shown to play a critical role in the protection against T1D. Thus, SomatoKine is a promising therapeutic approach in the treatment of T1D.

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Accession: 035980542

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