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Akt/PKB activation and insulin signaling: a novel insulin signaling pathway in the treatment of type 2 diabetes

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Figure

Figure 1 Insulin and contraction signaling pathways during GLUT-4 recruitment and translocation.Note: Data from Sakamoto et al.14Abbreviations: IRS, insulin receptor substrate; PI3-K, class IA phosphatidylinositol 3-kinase; PIP2, phosphatidylinositol (4,5)-bisphosphate; PIP3, phosphatidylinositol 3,4,5-trisphosphate; PDK1, phosphoinositide-dependent protein kinase-1; Akt, serine/threonine protein kinase; AS160, 160 kDa Akt substrate; GLUT-4, glucose transporter 4;  GSV, GLUT-4 storage vesicle; Rab-GAP, Rab-GTPase-activating protein; Rab-GDP, guanosine-50-diphosphate-loaded Rab; Rab-GTP, guanosine-50-triphosphate-loaded Rab; CaMKK, Ca2+/calmodulin-dependent protein kinase kinase; LKB1, Serine/threonine kinase 11; STRAD, putative kinase; MO25, mouse protein 25/scaffold protein; AMPK, 5′-monophosphate-activated protein kinase; Thr172, phosphorylated AMPKα at threonine 172; AMP, adenosine monophosphate; ATP, adenosine triphosphate; P, phosphorylated site.
Figure 2 Inositol phosphates and Akt/PKB inhibition, a potential Akt/PKB feedback mechanism.Note: Adapted from Cell, 143(6), Manning BD, Insulin signaling: inositol phosphates get into the Akt, 861–863

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