Yang TT, Liu IM, Wu HT, Cheng JT
Mediation of Protein Kinase C zeta in mu-Opioid Receptor Activation for Increase of Glucose Uptake into Cultured Myoblast C(2)C(12) Cells. [JOURNAL ARTICLE]
Neurosci Lett 2009 Aug 11.
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 preincubated with GF 109203X 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.
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