Pekala P, Kawakami M, Vine W, Lane M D, Cerami A
J Exp Med. 1983 Apr 1;157(4):1360-5. doi: 10.1084/jem.157.4.1360.
An apparent insulin resistance is noted in 3T3-L1 adipocytes after the addition of an endotoxin-induced mediator from macrophages. Examination at the level of the insulin receptor has revealed that the mediator does not effect either the functional ability of the cells to bind insulin or the ability of insulin to stimulate the uptake of glucose. The resistance appears to reflect a post-receptor interference with the insulin-induced biosynthesis of the anabolic enzymes, acetyl Co-A carboxylase and fatty acid synthetase, which are required for the conversion of glucose into storage lipid. These studies offer a new in vitro model for investigating the molecular basis of insulin resistance.
在添加来自巨噬细胞的内毒素诱导介质后,3T3-L1脂肪细胞中出现明显的胰岛素抵抗。在胰岛素受体水平进行的检查显示,该介质既不影响细胞结合胰岛素的功能能力,也不影响胰岛素刺激葡萄糖摄取的能力。这种抵抗似乎反映了受体后对胰岛素诱导的合成代谢酶(乙酰辅酶A羧化酶和脂肪酸合成酶)生物合成的干扰,这些酶是将葡萄糖转化为储存脂质所必需的。这些研究为研究胰岛素抵抗的分子基础提供了一种新的体外模型。