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

Ting Ting Yang, I. Min Liu, Hung Tsung Wu, Juei Tang Cheng

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The present study is designed to investigate the role of atypical protein kinase C (PKC) in the signaling of μ-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 (ζ) 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-ζ 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-ζ in MOR signaling for glucose uptake in C2C12 cells. Activation of PKC-ζ by MOR stimulation is highly relevant to the search for therapeutic targets for glucose transport in insulin-sensitive tissues.

Original languageEnglish
Pages (from-to)177-180
Number of pages4
JournalNeuroscience Letters
Volume465
Issue number2
DOIs
Publication statusPublished - Nov 13 2009
Externally publishedYes

Keywords

  • μ-Opioid receptors
  • CC cells
  • Loperamide
  • Protein kinase C-ζ

ASJC Scopus subject areas

  • Neuroscience(all)

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