FEBS Letters · 1997 · 220 citations · 33 references
Life SciencesBiochemistryCell BiologyCell SignalingMetabolismSignal TransductionAdipose TissueCarbohydrate MetabolismDiabetes MellitusGlycogen MetabolismInsulin Signaling In MetabolismMetabolic SignalingGlycogen Regulation By InsulinGlycogen Synthase Kinase 3 RegulationGlycogen Synthase Kinase 3 SignalingGlycogen Synthase Kinase RegulationGlycogen Synthesis RegulationInsulin Signaling PathwayProtein Kinase B SignalingSkeletal Muscle Physiology
Insulin stimulated protein kinase B alpha (PKB alpha) more than 10-fold and decreased glycogen synthase kinase-3 (GSK3) activity by 50 +/- 10% in skeletal muscle and adipocytes. Rapamycin did not prevent the activation of PKB, inhibition of GSK3 or stimulation of glycogen synthase up to 5 min. Thus rapamycin-insensitive pathways mediate the acute effect of insulin on glycogen synthase in the major insulin-responsive tissues. The small and very transient effects of EGF on phosphatidylinositol (3,4,5)P3 PKB alpha and GSK3 in adipocytes, compared to the strong and sustained effects of insulin, explains why EGF does not stimulate glucose uptake or glycogen synthesis in adipocytes.
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Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B
Darren A.E. Cross, Dario R. Alessi, Philip Cohen et al. · Nature · 1995 · 5.2K citations