肿瘤坏死因子α和白细胞介素6致脂肪细胞胰岛素抵抗的不同机制

Tumor necrosis factor-α and interleukin-6 induced insulin resistance in adipocytes via distinct mechanisms

白细胞介素6（IL-6）和肿瘤坏死因子α（TNF-α）分别作用于3T3-L1细胞6h72h，观察对葡萄糖摄取和胰岛素信号转导的影响。两者作用72h抑制胰岛素刺激的葡萄糖摄取、胰岛素受体底物1（IRS-1）酪氨酸及蛋白激酶B（PKB）磷酸化，并使IRS-1表达下降。TNF-α作用6h增加IRS-1丝氨酸307磷酸化。提示IL-6和TNF-α致胰岛素抵抗的作用机制不尽相同。

3T3-L1 adipocytes were exposed separately to TNF-α and IL-6 for 6 or 72 h and glucose uptake and insulin signaling transduction in these ceils were measured. Both IL-6 and TNF-α treatments for 72 h inhibited insulin-stimulated glucose uptake, tyrosine phosphorylations of insulin receptor substrate-1 （ IRS-1 ） and protein kinase B （PKB） phosphorylation, and IRS-1 expression. Treatment with TNF-α for 6 h had no effect on IRS-1 expression but significantly increased Serine307 phosphorylation of SRS-1. Hence, IL-6 and TNF-α may induce insulin resistance via different mechanisms.