Mediation of protein kinase C zeta in μ-opioid receptor activation for increase of glucose uptake into cultured myoblast C2C12 cells

The present Study is designed to investigate the role of atypical protein kinase C(PKC) in the signaling of mu-opioid receptors (MOR) for glucose uptake in myoblast C2C12 cells Loperamide enhanced the uptake of radioactive deoxyglucose into C2C12 Cells in a concentration-dependent manner that was abolished in cells pre-incubated with GF109203X at concentrations sufficient to block PKC Inhibition of the atypical zeta (zeta) isoform of PKC using myristoylated PKC pseudosubstrate resulted in a concentration-dependent decrease of loperamide-stimulated glucose uptake into C2C12 cells In addition, loperamide elicited the phosphorylation of PKC-zeta in C2C12 cells in a concentration-dependent manner that was abolished by pretreatment with naloxonazine at concentrations sufficient to block MOR. These results suggest the mediation of PKC-zeta in MOR signaling for glucose uptake in C2C12 cells. Activation of PKC-zeta by MOR stimulation is highly relevant to the search for therapeutic targets for glucose transport in insulin-sensitive tissues (c) 2009 Elsevier Ireland Ltd. All rights reserved