Defective Activation of Atypical Protein Kinase C ζ and λ by Insulin and Phosphatidylinositol-3,4,5-(PO4)3 in Skeletal Muscle of Rats Following High-Fat Feeding and Streptozotocin-Induced Diabetes

1) muscle aPKCs are activated at relatively low, presumably physiological, as well as higher supraphysiological, insulin concentrations; 2) aPKC activation is defective in muscles of high-fat-fed and STZ-diabetic rats; and 3) defective aPKC activation in these states is at least partly due to impaired responsiveness to PI-3,4,5-(PO(4))(3), apparently at activation steps distal to PDK-1-dependent loop phosphorylation.