| First Author | Wueest S | Year | 2010 |
| Journal | FEBS Lett | Volume | 584 |
| Issue | 19 | Pages | 4187-92 |
| PubMed ID | 20828573 | Mgi Jnum | J:164421 |
| Mgi Id | MGI:4833880 | Doi | 10.1016/j.febslet.2010.08.052 |
| Citation | Wueest S, et al. (2010) Fas activation in adipocytes impairs insulin-stimulated glucose uptake by reducing Akt. FEBS Lett 584(19):4187-92 |
| abstractText | Fas (CD95) belongs to the superfamily of the tumor necrosis factor (TNF) receptors. Besides its key role in apoptosis, Fas contributes to non-apoptotic pathways such as cell proliferation and inflammation. In 3T3-L1 adipocytes, activation of Fas by Fas ligand decreased insulin-stimulated glucose uptake, without affecting cell viability. This decrease in glucose uptake was accompanied by reduced protein expression and diminished phosphorylation of Akt. Similarly, insulin-stimulated glucose incorporation and protein levels of Akt were increased in isolated adipocytes from Fas deficient mice when compared to wild-type mice. In conclusion, Fas activation in adipocytes decreases Akt expression and thereby impairs insulin sensitivity. |
