Division of Pediatric Endocrinology and Diabetology, University Children's Hospital, Zurich, Switzerland.
FEBS Lett. 2010 Oct 8;584(19):4187-92. doi: 10.1016/j.febslet.2010.08.052. Epub 2010 Sep 7.
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.
Fas（CD95）属于肿瘤坏死因子（TNF）受体超家族。除了在细胞凋亡中的关键作用外，Fas 还参与非细胞凋亡途径，如细胞增殖和炎症。在 3T3-L1 脂肪细胞中，Fas 配体激活 Fas 会降低胰岛素刺激的葡萄糖摄取，而不影响细胞活力。葡萄糖摄取的减少伴随着 Akt 的蛋白表达减少和磷酸化减少。同样，与野生型小鼠相比，从 Fas 缺陷型小鼠分离的脂肪细胞中，胰岛素刺激的葡萄糖摄取和 Akt 的蛋白水平增加。总之，脂肪细胞中 Fas 的激活会降低 Akt 的表达，从而损害胰岛素敏感性。
