【摘要】目的观察脂肪因子补体C1q/肿瘤坏死因子相关蛋白3(CTRP3)对 IR的3T3-L1脂肪细胞胰岛素信号通路的影响。方法以软脂酸培养构建IR的3T3-L1脂肪细胞模型，分为对照组、CTRP3(10、50、250ng/ml)干预组及CTRP3(250ng/ml)+ 渥曼青霉素(wortmannin)[磷脂酰肌醇3激酶(PI3K)抑制剂]干预组。以葡萄糖氧化酶法检测葡萄糖消耗量，以Westernblot检测PI3K及蛋白激酶B[PKB(ser437)]蛋白相对表达量。结果与对照组相比，CTRP3干预组(10、50、250ng/ml)葡萄糖消耗量分别增加了22.1%、42.9%及76.6%(P均<0.01)，PI3K蛋白相对表达量分别增加了62.5%、100.0%及137.5%(均P<0.01)，PKB(ser437)蛋白相对表达量分别增加了46.4%、160.7%及192.9%(P均<0.01);与CTRP3(250ng/ml)干预组相比，CTRP3(250ng/ml)+Wortmannin干预组葡萄糖消耗量下降53.2%(P<0.01)，PI3K及PKB(ser437)蛋白相对表达量分别下降了43.4%及56.1%(P均<0.01)。结论脂肪因子CTRP3可能通过改善胰岛素信号转导增加IR的3T3-L1脂肪细胞IS。

　　【关键词】脂肪因子补体C1q/肿瘤坏死因子相关蛋白3;胰岛素抵抗;3T3-L1脂肪细胞;胰岛素信号转导

　　【Abstact】Objective To investigate the impacts of C1q/TNF related protein-3 (CTRP3) on the insulin signal transduction of insulin resistant 3T3-L1 adipocytes. Methods The insulin resistant 3T3-L1 adipocytes were induced by palmitic acid(PA), and were divided into control group, CTRP3(10,50,250 ng/ml) intervention group and CTRP3(250 ng/ml)+wortmannin [phosphatidylinositol-4,5- bisphosphate 3-kinase (PI3K) inhibitor]intervention group. The glucose consumption was detected by glucose oxidase method. The relative protein expression level of insulin signal molecules were detected by western-blot. Results Compared with control group, the glucose consumption of CTRP3(10,50,250 ng/ml) intervention group was increased by 22.1%, 42.9% and 76.6%, respectively(all P<0.01), the relative protein expression level of PI3K and PKB(ser437) was increased by 62.5% and 46.4%,100.0% and160.7% and 137.5% and 192.9%, respectively(all P <0.01) . Compared with CTRP3(250 ng/ml) intervention group, the glucose consumption of CTRP3(250 ng/ml)+wortmannin intervention group was decreased by 53.2%(P<0.01), the relative protein expression level of PI3K and PKB(ser437) was decreased by 43.4% and 56.1%, respectively (all P <0.01). Conclusion CTRP3 may increase the insulin sensitivity of insulin resistant 3T3-L1 adipocytes by enhancing insulin signal transduction.

　　【Key words】 C1q/TNF related protein 3; Insulin resistance(CTRP3); 3T3-L1 adipocyte; Insulin signal transduction