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

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Deletion of Gab1 in the liver leads to enhanced glucose tolerance and improved hepatic insulin action.

Insulin receptor substrate-1 (IRS-1) and IRS-2 are known to transduce and amplify signals emanating from the insulin receptor. Here we show that Grb2-associated binder 1 (Gab1), despite its structural similarity to IRS proteins, is a negative modulator of hepatic insulin action. Liver-specific Gab1 knockout (LGKO) mice showed enhanced hepatic insulin sensitivity with reduced glycemia and improved glucose tolerance. In LGKO liver, basal and insulin-stimulated tyrosine phosphorylation of IRS-1 and IRS-2 was elevated, accompanied by enhanced Akt/ PKB activation. Conversely, Erk activation by insulin was suppressed in LGKO liver, leading to defective IRS-1 Ser612 phosphorylation. Thus, Gab1 acts to attenuate, through promotion of the Erk pathway, insulin-elicited signals flowing through IRS and Akt proteins, which represents a novel balancing mechanism for control of insulin signal strength in the liver.[1]

References

  1. Deletion of Gab1 in the liver leads to enhanced glucose tolerance and improved hepatic insulin action. Bard-Chapeau, E.A., Hevener, A.L., Long, S., Zhang, E.E., Olefsky, J.M., Feng, G.S. Nat. Med. (2005) [Pubmed]
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