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Essential role of protein kinase Cζ in the impairment of insulin-induced glucose transport in IRS-2-deficient brown adipocytes

AuthorsArribas, Mónica; Valverde, Ángela M.; Burks, Deborah J.; Benito, Manuel
KeywordsInsulin receptor substrate-2
Glucose transport
Protein kinase C
Issue Date2003
CitationFEBS Letters 536(1-3): 161-166 (2003)
AbstractInsulin receptor substrate-2-deficient (IRS-2-/-) mice develop type 2 diabetes. We have investigated the molecular mechanisms by which IRS-2-/- immortalized brown adipocytes showed an impaired response to insulin in inducing GLUT4 translocation and glucose uptake. IRS-2-associated phosphatidylinositol 3-kinase (PI 3-kinase) activity was blunted in IRS-2-/- cells, total PI 3-kinase activity being reduced by 30%. Downstream, activation of protein kinase C (PKC) ζ was abolished in IRS-2-/- cells. Reconstitution with retroviral IRS-2 restores IRS-2/PI 3-kinase/PKCζ signalling, as well as glucose uptake. Wild-type cells expressing a kinase-inactive mutant of PKCζ lack GLUT4 translocation and glucose uptake. Our results support the essential role played by PKCζ in the insulin resistance and impaired glucose uptake observed in IRS-2-deficient brown adipocytes.
Identifiersdoi: 10.1016/S0014-5793(03)00049-8
issn: 0014-5793
e-issn: 1873-3468
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