补体C1q／肿瘤坏死因子相关蛋白3对3T3-L1脂肪细胞脂肪因子表达的影响

目的：观察脂肪因子补体C1q/肿瘤坏死因子（TNF）相关蛋白3（CTRP3）对3T3-L1脂肪细胞脂联素（APN）、瘦素（LPT）、内脏脂肪素（VFT）及爱帕琳肽（APL）等脂肪因子表达的调节效应，以及胰岛素抵抗对该调节效应的影响。方法以软脂酸诱导胰岛素抵抗的3 T3-L1脂肪细胞模型，分别以10、50、250μg/L CTRP3干预正常3T3-L1脂肪细胞12以及250μg/L CTRP3干预胰岛素抵抗的3T3-L1脂肪细胞12 h。分别通过酶联免疫吸附法（ ELISA）及实时定量-聚合酶链反应（ RT-PCR）法检测脂肪因子蛋白分泌量及基因表达水平。组间差异采用方差分析，两组间进一步比较采用SNK-q检验。结果250μg/L CTRP3干预正常组APN、LPT、VFT及APL蛋白分泌量较正常对照组分别增加了63.3％、42.9％、57.1％及56.0％（ q＝8.605、8.526、8.284、8.573，均 P＜0.05）；10及50μg/L干预组上述脂肪因子蛋白分泌量呈增加趋势，但除50μg/L CTRP3干预组APL蛋白分泌量较对照组显著增加外（6.2＆#177;1.1）比（5.0＆#177;0.9）μg/L， q＝4.593，P＜0.05]，其余均差异无统计学意义（均P＞0.05）；其基因表达变化趋势与此类似，并且在干预浓度为50μg/L时APN、LPT、VFT及APL mRNA表达水平较正常对照组分别增加22.0％、13.0％、20.0％及33.0％（ q＝6.150、3.987、5.653、9.031，均P＜0.05）。与CTRP3（250μg/L）干预正常脂肪细胞相比，CTRP3（250μg/L）干预胰岛素抵抗脂肪细胞APN、LPT、VFT及APL蛋白分泌量分别降低了28.6％、21.0％、24.5％及17.9％（ q＝6.341、5.969、5.592、4.287，均 P ＜0.05），基因表达降低了21.6％、17.2％、15.6％及18.9％（q ＝9.225、7.668、7.066、8.210，均P＜0.05）。结论 CTRP3浓度依赖性地增加3T3-L1脂肪细胞APN、LPT、VFT及APL的表达，胰岛素抵抗降低该调节效应。

Effects of C1q/tumor necrosis factor related protein-3 on the expression of adipokines in 3T3-L1 adipocytes

Objective To investigate the impacts of C1q/tumor necrosis factor （TNF） related protein-3 （ CTRP3 ） on the expression of adiponectin （ APN ） , leptin （ LPT ） , visfatin （ VFT ） and apelin （APL） in 3T3-L1 adipocytes.The effect of insulin resistance on the impacts was also investigated.Methods The insulin resistant 3T3-L1 adipocytes were induced by palmic acid.There were six groups：normal control group, insulin resistance group, CTRP3（10,50,250 μg/L） treated normal group and CTRP3 （250 μg/L） treated insulin resistance group.The secretion and gene expression of the adipokines were detected by enzyme-linked immunosorbent assay （ ELISA ） and real-time polymerase chain reaction （ RT-PCR ） respectively.One-way ANOVA was used for statistical analysis of the differences among groups and SNK-q test was used for the further comparison between two groups.Results Compared with normal control group , the secretion of APN , LPT, VFT and APL in 250 μg/ml CTRP3 intervention group was increased by 63.3%, 42.9%, 57.1%and 56.0%（ q=8.605,8.526,8.284,8.573,all P〈0.05） respectively.The secretion of such adipokines had increased trend in 10 and 50 μg/L CTRP3 intervention groups , while only the increase of APL in 50 μg/L CTRP3 intervention group was significant （ （ 6.2 ±1.1 ） vs （ 5.0 ±0.9 ）μg/L, q=4.593, P〈0.05）.The gene expression had the same trend after treatment , and the mRNA relative expression of APN , LPT, VFT and APL at the intervention concentration of 50 μg/L was increased＆amp;nbsp;by 22.0%, 13.0%, 20.0%and 33.0%respectively in comparison with that in normal control group （ q=6.150, 3.987, 5.653, 9.031, all P〈0.05）.Compared with the CTRP3 treated normal group, the protein release of APN , LPT, VFT and APL in CTRP3 treated insulin resistant group were decreased by 28.6%, 21.0%, 24.5%and 17.9%respectively （q=6.341, 5.969, 5.592, 4.287, all P〈0.05）, and gene expression were decreased by 21.6%, 17.2%, 15.6% and 18.9% respectively （ q =9.225, 7