| First Author | Ko WC | Year | 2006 |
| Journal | Neurosci Lett | Volume | 397 |
| Issue | 3 | Pages | 274-8 |
| PubMed ID | 16406665 | Mgi Jnum | J:108017 |
| Mgi Id | MGI:3622858 | Doi | 10.1016/j.neulet.2005.12.047 |
| Citation | Ko WC, et al. (2006) Effect of opioid mu-receptors activation on insulin signals damaged by tumor necrosis factor alpha in myoblast C2C12 cells. Neurosci Lett 397(3):274-8 |
| abstractText | In an attempt to develop a new target for handling of insulin resistance, we investigated the effect of opioid mu-receptor activation on insulin signals in differentiated myoblast C2C12 cells damaged by tumor necrosis factor-alpha (TNFalpha). A marked reduction of insulin-stimulated radioactive 2-deoxyglucose (2-DG) uptake was observed in TNFalpha (10 ng/ml for 1 h)-treated cells. Loperamide (10 micromol/l for 24 h) reversed the inhibition of insulin-stimulated 2-DG uptake by TNFalpha in a manner sensitive to blockade of opioid mu-receptors. Insulin signals damaged by TNFalpha were the impaired expressions of insulin receptor (IR), tyrosine autophosphorylation in IR, and insulin receptor substrate (IRS)-1 protein, as well as a decrease of IRS-1 tyrosine phosphorylation. Also, the signaling defects including an attenuated p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3-kinase) and Akt serine phosphorylation were observed. Loperamide (10 micromol/l for 24 h) reversed the TNFalpha-induced decrement of insulin signals at same concentration used to raise glucose uptake. In conclusion, activation of opioid mu-receptors may reverse the insulin signals damaged by inflammatory cytokine. |
