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Deficiency of a β-arrestin-2 signal complex contributes to insulin resistance

Author

Listed:
  • Bing Luan

    (Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, and Graduate School of the Chinese Academy of Sciences,)

  • Jian Zhao

    (Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, and Graduate School of the Chinese Academy of Sciences,)

  • Haiya Wu

    (Shanghai Jiaotong University Affiliated Sixth People’s Hospital; Shanghai Clinical Center of Diabetes, 200233, Shanghai, China
    Shanghai Diabetes Institute)

  • Baoyu Duan

    (Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, and Graduate School of the Chinese Academy of Sciences,)

  • Guangwen Shu

    (Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, and Graduate School of the Chinese Academy of Sciences,)

  • Xiaoying Wang

    (Fudan University Affiliated Zhongshan Hospital, 200032, Shanghai, China)

  • Dangsheng Li

    (Shanghai Information Center for Life Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 200031, Shanghai, China)

  • Weiping Jia

    (Shanghai Jiaotong University Affiliated Sixth People’s Hospital; Shanghai Clinical Center of Diabetes, 200233, Shanghai, China
    Shanghai Diabetes Institute)

  • Jiuhong Kang

    (Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, and Graduate School of the Chinese Academy of Sciences,)

  • Gang Pei

    (Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, and Graduate School of the Chinese Academy of Sciences,
    School of Life Science and Technology, Tongji University, 200092, Shanghai, China)

Abstract

Insulin signalling derailed The insulin resistance characteristic of type 2 diabetes and obesity is caused by the failure of insulin to stimulate receptor signalling. Defining the cellular mechanisms of this defect is critical to understanding these disorders. Experiments in type 2 diabetes clinical samples and mouse models now show that the scaffold protein β-arrestin-2 is necessary for efficient insulin signalling, linking the downstream kinases Akt and Src to the insulin receptor. β-arrestin-2 is downregulated both in diabetic mice and in patients. Without β-arrestin-2, insulin resistance develops, and reinstating its expression restores insulin sensitivity in mice. This suggests possible new therapeutic targets in insulin resistance and its related disorders.

Suggested Citation

  • Bing Luan & Jian Zhao & Haiya Wu & Baoyu Duan & Guangwen Shu & Xiaoying Wang & Dangsheng Li & Weiping Jia & Jiuhong Kang & Gang Pei, 2009. "Deficiency of a β-arrestin-2 signal complex contributes to insulin resistance," Nature, Nature, vol. 457(7233), pages 1146-1149, February.
    • Handle: RePEc:nat:nature:v:457:y:2009:i:7233:d:10.1038_nature07617
    DOI: 10.1038/nature07617
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