CAJ | 학술논문

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±1.1）比（5.0±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。
목적：관찰지방인자보체C1q/종류배사인자（TNF）상관단백3（CTRP3）대3T3-L1지방세포지련소（APN）、수소（LPT）、내장지방소（VFT）급애파림태（APL）등지방인자표체적조절효응，이급이도소저항대해조절효응적영향。방법이연지산유도이도소저항적3 T3-L1지방세포모형，분별이10、50、250μg/L CTRP3간예정상3T3-L1지방세포12이급250μg/L CTRP3간예이도소저항적3T3-L1지방세포12 h。분별통과매련면역흡부법（ ELISA）급실시정량-취합매련반응（ RT-PCR）법검측지방인자단백분비량급기인표체수평。조간차이채용방차분석，량조간진일보비교채용SNK-q검험。결과250μg/L CTRP3간예정상조APN、LPT、VFT급APL단백분비량교정상대조조분별증가료63.3％、42.9％、57.1％급56.0％（ q＝8.605、8.526、8.284、8.573，균 P＜0.05）；10급50μg/L간예조상술지방인자단백분비량정증가추세，단제50μg/L CTRP3간예조APL단백분비량교대조조현저증가외[（6.2±1.1）비（5.0±0.9）μg/L， q＝4.593，P＜0.05]，기여균차이무통계학의의（균P＞0.05）；기기인표체변화추세여차유사，병차재간예농도위50μg/L시APN、LPT、VFT급APL mRNA표체수평교정상대조조분별증가22.0％、13.0％、20.0％급33.0％（ q＝6.150、3.987、5.653、9.031，균P＜0.05）。여CTRP3（250μg/L）간예정상지방세포상비，CTRP3（250μg/L）간예이도소저항지방세포APN、LPT、VFT급APL단백분비량분별강저료28.6％、21.0％、24.5％급17.9％（ q＝6.341、5.969、5.592、4.287，균 P ＜0.05），기인표체강저료21.6％、17.2％、15.6％급18.9％（q ＝9.225、7.668、7.066、8.210，균P＜0.05）。결론 CTRP3농도의뢰성지증가3T3-L1지방세포APN、LPT、VFT급APL적표체，이도소저항강저해조절효응。
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 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, 7.668, 7.066, 8.210, all P<0.05).Conclusion CTRP3 may dose-dependently increase the secretion and gene expression of APN, LPT, VFT and APL in 3T3-L1 adipocytes.Insulin resistance may inhibit this effect.