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

Bing Luan, Jian Zhao, Haiya Wu, Baoyu Duan, Guangwen Shu, Xiaoying Wang, Dangsheng Li, Weiping Jia, Jiuhong Kang and Gang Pei ()
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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
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
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,

Nature, 2009, vol. 457, issue 7233, 1146-1149

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.

Date: 2009
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DOI: 10.1038/nature07617

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