| First Author | Yang TT | Year | 2009 |
| Journal | Neurosci Lett | Volume | 465 |
| Issue | 2 | Pages | 177-80 |
| PubMed ID | 19682542 | Mgi Jnum | J:155169 |
| Mgi Id | MGI:4412419 | Doi | 10.1016/j.neulet.2009.08.026 |
| Citation | Yang TT, et al. (2009) Mediation of protein kinase C zeta in mu-opioid receptor activation for increase of glucose uptake into cultured myoblast C2C12 cells. Neurosci Lett 465(2):177-80 |
| abstractText | 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. |
