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

被引：15
|
作者：
Yang, Ting-Ting [2 ]
Liu, I-Min [3 ,4 ]
Wu, Hung-Tsung [1 ]
Cheng, Juei-Tang [1 ,5 ]
机构：
[1] Natl Cheng Kung Univ, Inst Basic Med Sci, Coll Med, Dept Pharmacol, Tainan 70101, Taiwan
[2] China Med Univ, Coll Med, Grad Inst Basic Med Sci, Taichung 40401, Taiwan
[3] Tajen Univ, Dept Pharm, Yen Pou 90701, Ping Tung Shien, Taiwan
[4] Tajen Univ, Grad Inst Pharmaceut Technol, Yen Pou 90701, Ping Tung Shien, Taiwan
[5] Chi Mei Med Ctr, Dept Med Res, Yung Kang 73101, Tainan Hsien, Taiwan
来源：
NEUROSCIENCE LETTERS | 2009年 / 465卷 / 02期
关键词：
C2C12; cells; Loperamide; mu-Opioid receptors; Protein kinase C-zeta; INDUCED DIABETIC-RATS; HUMAN SKELETAL-MUSCLE; TRANSPORT;
D O I：
10.1016/j.neulet.2009.08.026
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
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
引用
收藏
页码：177 / 180
页数：4
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