Insulin modulates gluconeogenesis by inhibition of the coactivator TORC2

Renaud Dentin, Yi Liu, Seung-Hoi Koo, Susan Hedrick, Thomas Vargas, Jose Heredia, John Yates and Marc Montminy ()
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Renaud Dentin: Peptide Biology Laboratories, Salk Institute For Biological Studies, La Jolla, California 92037, USA
Yi Liu: Peptide Biology Laboratories, Salk Institute For Biological Studies, La Jolla, California 92037, USA
Seung-Hoi Koo: Sungkyunkwan University School of Medicine, 300 Chunchun-dong, Jangan-gu, Suwon, 440-746, Gyeonggi-do, Korea
Susan Hedrick: Peptide Biology Laboratories, Salk Institute For Biological Studies, La Jolla, California 92037, USA
Thomas Vargas: Peptide Biology Laboratories, Salk Institute For Biological Studies, La Jolla, California 92037, USA
Jose Heredia: Peptide Biology Laboratories, Salk Institute For Biological Studies, La Jolla, California 92037, USA
John Yates: The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
Marc Montminy: Peptide Biology Laboratories, Salk Institute For Biological Studies, La Jolla, California 92037, USA

Nature, 2007, vol. 449, issue 7160, 366-369

Abstract: TORC2 and diabetes A previously unrecognized pathway by which insulin modulates hepatic glucose production is described in this issue. Glucose levels are maintained within a narrow range in mammals through the effects of pancreatic hormones on liver gluconeogenesis. This new pathway facilitates the inhibition of the expression of gluconeogenic genes by insulin by promoting the phosphorylation and ubiquitin-dependent degradation of the CREB coactivator TORC2. The signalling pathway involves the kinase SIK2 and the E3 ligase COP1. The findings point to TORC2 and SIK2 as potential therapeutic targets in type II diabetes.

Date: 2007
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DOI: 10.1038/nature06128

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