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    EMBO Rep. 2011 Jul 1;12(8):847-54. doi: 10.1038/embor.2011.108.

    The association of phosphoinositide 3-kinase enhancer A with hepatic insulin receptor enhances its kinase activity.

    Chan CB, Liu X, He K, Qi Q, Jung DY, Kim JK, Ye K.

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    Department of Pathology and Laboratory Medicine, Emory University School of Medicine, 615 Michael Street, Atlanta, Georgia 30322, USA.

    Abstract

    Dysfunction of hepatic insulin receptor tyrosine kinase (IRTK) causes the development of type 2 diabetes. However, the molecular mechanism regulating IRTK activity in the liver remains poorly understood. Here, we show that phosphoinositide 3-kinase enhancer A (PIKE-A) is a new insulin-dependent enhancer of hepatic IRTK. Liver-specific Pike-knockout (LPKO) mice display glucose intolerance with impaired hepatic insulin sensitivity. Specifically, insulin-provoked phosphoinositide 3-kinase/Akt signalling is diminished in the liver of LPKO mice, leading to the failure of insulin-suppressed gluconeogenesis and hyperglycaemia. Thus, hepatic PIKE-A has a key role in mediating insulin signal transduction and regulating glucose homeostasis in the liver.

    PMID:
    21720388
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC3147257
    [Available on 2012/8/1]

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