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Abstract
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
C(2)C(12) cells. Loperamide enhanced the uptake of radioactive deoxyglucose into C(2)C(12)
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 C(2)C(12) cells. In addition,
loperamide elicited the phosphorylation of PKC-zeta in C(2)C(12) 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 C(2)C(12) cells. Activation of PKC-zeta by MOR stimulation is highly
relevant to the search for therapeutic targets for glucose transport in insulin-sensitive
tissues.