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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Granuphilin is activated by SREBP-1c and involved in impaired insulin secretion in diabetic mice.

Granuphilin is a crucial component of the docking machinery of insulin-containing vesicles to the plasma membrane. Here, we show that the granuphilin promoter is a target of SREBP-1c, a transcription factor that controls fatty acid synthesis, and MafA, a beta cell differentiation factor. Potassium-stimulated insulin secretion (KSIS) was suppressed in islets with adenoviral-mediated overexpression of granuphilin and enhanced in islets with knockdown of granuphilin (in which granuphilin had been knocked down). SREBP-1c and granuphilin were activated in islets from beta cell-specific SREBP-1c transgenic mice, as well as in several diabetic mouse models and normal islets treated with palmitate, accompanied by a corresponding reduction in insulin secretion. Knockdown- or knockout-mediated ablation of granuphilin or SREBP-1c restored KSIS in these islets. Collectively, our data provide evidence that activation of the SREBP-1c/granuphilin pathway is a potential mechanism for impaired insulin secretion in diabetes, contributing to beta cell lipotoxicity.[1]

References

  1. Granuphilin is activated by SREBP-1c and involved in impaired insulin secretion in diabetic mice. Kato, T., Shimano, H., Yamamoto, T., Yokoo, T., Endo, Y., Ishikawa, M., Matsuzaka, T., Nakagawa, Y., Kumadaki, S., Yahagi, N., Takahashi, A., Sone, H., Suzuki, H., Toyoshima, H., Hasty, A.H., Takahashi, S., Gomi, H., Izumi, T., Yamada, N. Cell metabolism. (2006) [Pubmed]
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