AIM:To investigate the effects of C1q/TNF related protein 3 (CTRP3) on the insulin sensitivity of insulin resistant 3T3-L1 adipocytes.METHODS: The insulin resistance model of 3T3-L1 adipocytes was induced by palmic acid cultivation.The adipocytes were treated with different concentrations of recombinant CTRP3 protein (10, 50, 250,1 250 μg/L) for 12 h, and for different times (2, 6, 12, 24 h) at the concentration of 250μg/L.The glucose con-sumption was detected by the glucose oxidase method.The glucose transport ratio was measured by 2-deoxidation-[3H]-glucose intake method.The contents of TNF-αand IL-6 in the supernatant were detected by ELISA.The mRNA expression of TNF-α, IL-6 and glucose transporter-4 (GLUT-4) was measured by real-time PCR.The protein expression of GLUT-4 was detected by Western blotting.RESULTS:Compared with normal control ( NC) group, the glucose consumption and glucose intake ratio of insulin resistance ( IR) group was decreased by 50.6%and 57.9%, respectively.Compared with IR group, with the increase in CTRP3 (10, 50, 250,1 250 μg/L) in intervention groups, the glucose consumptions were in-creased by 22.1%, 42.9%, 76.6% and 80.5%, respectively, and the glucose intake ratios were increased by 39.0%, 68.0%, 108.0%and 111.0%, respectively.With the increased duration (2, 6, 12 and 24 h) of CTRP3 treatment at the concentration of 250 μg/L, the glucose intake ratio was increased by 23.0%, 79.0%, 109.0%and 114.0%, respectively. The contents of TNF-αand IL-6 in the supernatant were decreased by 17.4%and 17.1%respectively as treated with CTRP3 at the concentration of 250 μg/L for 12 h, and the mRNA expression of TNF-αand IL-6 was decreased by 26.0% and 18.9%respectively, while the mRNA and protein expression of GLUT-4 was increased by 61.5%and 55.6%respectively. CONCLUSION:CTRP3 may increase the insulin sensitivity of insulin resistant 3T3-L1 adipocytes by down-regulating the expression of inflammatory factors, improving the insulin signal transduction and increasing the expression of GLUT-4.%目的：观察脂肪因子C1q/TNF相关蛋白3（CTRP3）对胰岛素抵抗的3T3-L1脂肪细胞胰岛素敏感性的效应及机制。方法：通过软脂酸培养构建3 T3-L1脂肪细胞胰岛素抵抗模型，以不同浓度重组CTRP3蛋白（10、50、250、1250μg/L）干预12 h，以及250μg/L CTRP3干预不同时间（2、6、12、24 h），以葡萄糖氧化酶法检测葡萄糖消耗量，以2-脱氧-[3 H]-葡萄糖摄入法检测葡萄糖转运率，以酶联免疫吸附（ ELISA）法检测上清中肿瘤坏死因子α（TNF-α）及白细胞介素6（IL-6）的含量，以荧光实时定量PCR（real-time PCR）检测TNF-α、IL-6及葡萄糖转运子4（ GLUT-4）的mRNA表达水平，以Western blotting检测GLUT-4蛋白表达水平。结果：与正常对照组（ NC）相比，胰岛素抵抗组（IR）葡萄糖摄取率及葡萄糖消耗量分别降低了50．6％及57．9％（均P＜0．01）；与IR组相比，干预组随CTRP3浓度增加，葡萄糖消耗量分别增加22．1％、42．9％、76．6％及80．5％（均P＜0.01），葡萄糖摄取率分别增加39．0％、68．0％、108．0％及111．0％（均P＜0．01）；250μg/L CTRP3干预时间增加，葡萄糖摄取率分别增加23．0％、79．0％、109．0％及114．0％（均P＜0．01）；250μg/L CTRP3干预12 h，上清中的TNF-α及IL-6浓度分别降低了17．4％及17．1％（均P＜0．01），其mRNA相对表达量分别下降了26．0％及18．9％（均P＜0．01），而GLUT-4 mRNA及蛋白相对表达量分别增加了61．5％及55．6％（均P＜0.01）。结论： CTRP3具有改善胰岛素抵抗的3T3-L1脂肪细胞胰岛素敏感性的作用，其机制可能与下调炎症因子表达、改善胰岛素信号转导和增加葡萄糖转运子表达等有关。
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