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Diabetes 50:1244-1252, 2001
© 2001 by the American Diabetes Association, Inc.

Protein Kinase C (PKC)-{alpha} Activation Inhibits PKC-{zeta} and Mediates the Action of PED/PEA-15 on Glucose Transport in the L6 Skeletal Muscle Cells

Gerolama Condorelli, Giovanni Vigliotta, Alessandra Trencia, Maria Alessandra Maitan, Matilde Caruso, Claudia Miele, Francesco Oriente, Stefania Santopietro, Pietro Formisano, and Francesco Beguinot

Dipartimento di Biologia e Patologia Cellulare e Molecolare and the Centro di Endocrinologia ed Oncologia Sperimentale del C.N.R., Federico II University of Naples, Naples, Italy

Overexpression of the PED/PEA-15 protein in muscle and adipose cells increases glucose transport and impairs further insulin induction. Like glucose transport, protein kinase C (PKC)-{alpha} and -ß are also constitutively activated and are not further stimulatable by insulin in L6 skeletal muscle cells overexpressing PED (L6PED). PKC-{zeta} features no basal change but completely loses insulin sensitivity in L6PED. In these cells, blockage of PKC-{alpha} and -ß additively returns 2-deoxy-D-glucose (2-DG) uptake to the levels of cells expressing only endogenous PED (L6WT). Blockage of PKC-{alpha} and -ß also restores insulin activation of PKC-{zeta} in L6PED cells, with that of PKC-{alpha} sixfold more effective than PKC-ß. Similar effects on 2-DG uptake and PKC-{zeta} were also achieved by 50-fold overexpression of PKC-{zeta} in L6PED. In L6WT, fivefold overexpression of PKC-{alpha} or -ß increases basal 2-DG uptake and impairs further insulin induction with no effect on insulin receptor or insulin receptor substrate phosphorylation. In these cells, overexpression of PKC-{alpha} blocks insulin induction of PKC-{zeta} activity. PKC-ß is 10-fold less effective than PKC-{alpha} in inhibiting PKC-{zeta} stimulation. Expression of the dominant-negative K281->W PKC-{zeta} mutant simultaneously inhibits insulin activation of PKC-{zeta} and 2-DG uptake in the L6WT cells. We conclude that activation of classic PKCs, mainly PKC-{alpha}, inhibits PKC-{zeta} and may mediate the action of PED on glucose uptake in L6 skeletal muscle cells.


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