吡格列酮、TNF-α对3T3-L1细胞Perilipin mRNA表达影响的研究

目的探讨吡格列酮和TNF-α对3T3-L1细胞中perilipin（周脂素）mRNA表达的影响及其时间效应。方法用吡格列酮（100μmol.L-1）和TNF-α（100μg.L-1）分别处理未分化、分化过程中和分化成熟后的3T3-L1细胞,RT-PCR检测不同干预时间perilipin mRNA的表达水平。结果 （1）未分化3T3-L1细胞中perilipin未见表达,分化过程中细胞perilipin mRNA的表达水平随时间递增。（2）在分化过程中和分化成熟的3T3-L1细胞中,吡格列酮都明显增加perilipin mRNA的表达,TNF-α则明显抑制perilipin mRNA的表达。（3）吡格列酮能抵抗TNF-α对成熟3T3-L1脂肪细胞perilipin mRNA表达的抑制作用。结论随着分化成熟,3T3-L1细胞perilipin mRNA表达量逐渐增加;吡格列酮能明显增加3T3-L1细胞的perilipin mRNA表达,TNF-α则明显抑制其表达;吡格列酮能抵抗TNF-α对3T3-L1脂肪细胞perilipin mRNA表达的抑制作用。     

吡格列酮对3T3-L1细胞分化过程中perilipin基因表达的影响

脂肪组织不仅仅是被动的能量储存器官，而且是能够分泌多种激素类物质的内分泌器。脂肪细胞分化及其调控失常与人类多种疾病如肥胖症、胰岛素抵抗及2型糖尿病等密切相关。Pefilipin（围脂素）是新近发现的特异表达于脂肪细胞和类固醇生成细胞脂滴表面的一种磷蛋白，其基因受PPARV（过氧化物酶体增殖物激活受体）调控。国外有报道认为，pefilipin基因有随3T3-L1脂肪细胞分化成熟表达水平逐渐升高的趋势，提示该基因可能与肥胖的病理生理过程有关。噻唑烷二酮类药物吡格列酮作为PPAR1配体，对肥胖患者的胰岛素抵抗状态有改善作用，而且具有促进脂肪细胞分化的作用特点；而目前国内有关吡格列酮对脂肪细胞中pefilipin基因表达的调节作用未见报道，因此本研究应用吡格列酮干预分化过程中3T3-L1细胞，观察3T3-L1细胞分化过程中pefilipin mRNA表达量的变化，探讨吡格列酮对perilipin mRNA表达的影响。     

吡格列酮衍生物CQMUHS-03对3T3-L1细胞增殖分化的影响

目的研究吡格列酮衍生物CQMUHS-03对3T3-L1细胞增殖及诱导分化的影响,为CQMUHS-03的临床应用提供理论基础。方法 (1)不同浓度药物处理细胞,于24、48、72h,MTT法检测CQMUHS-03对3T3-L1前脂肪细胞增殖的影响。(2)建立3T3-L1细胞诱导分化模型,药物处理后经油红O染色,拍照后并测定570 nm处光密度值以确定有效药物干预浓度。(3)Western blot测定药物对PPARγ蛋白表达的影响。(4)Real-time PCR分析PPARγ基因表达。结果(1)经24、48、72 h MTT检测,1×10-6mol·L-1浓度以下的CQMUHS-03对3T3-L1细胞增殖的抑制作用弱,IC50为3.33×10-4mol·L-1,高于吡格列酮(2.91×10-4mol·L-1)。(2)油红O染色测定结果显示吡格列酮促进3T3-L1前脂肪细胞分化,而CQMUHS-03对3T3-L1前脂肪细胞的分化促进作用不明显。(3)Real-time PCR检测显示诱导分化8 d,吡格列酮组PPARγmRNA表达上调5.12倍,CQMUHS-03组PPARγmRNA表达上调2.29倍。(4)Western blot结果显示,CQMUHS-03使PPARγ的表达增高。结论吡格列酮衍生物CQMUHS-03对3T3-L1细胞抑制增殖作用弱于吡格列酮,对细胞分化无明显促进作用,能上调PPARγ基因和蛋白表达。     

3T3-L1前脂肪细胞分化过程中miRNAs基因的表达变化

目的:探讨3T3-L1前脂肪细胞诱导分化过程中miRNAs基因的表达变化。方法:运用经典的"激素鸡尾酒"法建立3T3-L1前脂肪细胞分化模型。采用实时定量聚合酶链式反应方法检测不同时相点(0d、2h、2d、4d)细胞分化相关标志物的表达和20种miRNAs的表达变化,采用生物信息学方法对变化显著的miRNAs进行靶基因预测。结果:成功建立3T3-L1前脂肪细胞分化模型。不同时相点细胞分化相关标志物基因水平提示3T3-L1前脂肪细胞分化为脂肪细胞。20种miRNAs中以miR-126、miR-214、miR-320、miR-351的表达最为显著。靶基因预测结果显示,miR-126靶基因有影响细胞增殖的转录因子Crk、代谢相关基因Irs1等;miR-214靶基因有转录因子Zbtb20、Kpna1等;miR-320靶基因有影响代谢相关基因Igf2bp3、Gxylt1等;miR-351靶基因有Myt1、Mcl1、Bmf等。结论:miR-126、miR-214、miR-320、miR-351可通过影响基因转录及细胞代谢水平,从而对3T3-L1前脂肪细胞分化发挥作用,为开发治疗肥胖等疾病的新药提供了新的研究思路。     

太子参提取物对3T3-L1前脂肪细胞分化的影响

目的 探索太子参提取物对3 T3-L1前脂肪细胞分化的影响.方法 采用超声提取法获得太子参乙醇提取物,再分别用石油醚、乙酸乙酯、水饱和正丁醇进行连续萃取,用得到的太子参各溶剂萃取层作用于3 T3-L1前脂肪细胞分化模型,以罗格列酮为阳性对照药,并通过油红O染色观察其对前脂肪细胞分化过程的影响.结果 太子参乙醇提取物及各极性溶剂萃取层在0.4μg·mL-1和0.8μg·mL-1两个浓度下均能在一定程度上促进前脂肪细胞的分化过程,而且乙酸乙酯萃取层活性最强.结论 太子参乙酸乙酯萃取层具有较好的促进3 T3-L1前脂肪细胞分化的活性.     

小檗碱对3T3-L1前脂肪细胞增殖和分化的影响

脂肪细胞的增多是由于前脂肪细胞的不断分化引起。小檗碱是中药黄连的成分，具有改善胰岛素抵抗、降低血糖和调节血脂紊乱的作用，可用于治疗2型糖尿病，但它是否参与脂肪细胞的增殖和分化过程，目前尚不清楚。本研究通过小檗碱干预小鼠前脂肪细胞观察其对该细胞增殖和分化的影响，为肥胖的2型糖尿病的治疗提供可能的途径。     

海地瓜硫酸软骨素对3T3-L1前脂肪细胞增殖和分化的影响

目的研究海地瓜硫酸软骨素(Acaudina Molpadioideschondroitin sulfate,AM-CHS)对3T3-L1前脂肪细胞增殖和分化的影响,并探讨其作用机制。方法采用传统的鸡尾酒诱导剂诱导分化3T3-L1前脂肪细胞,以MTT法检测AM-CHS对3T3-L1前脂肪细胞及不同分化阶段3T3-L1细胞增殖活性的影响;分别采用油红O染色和甘油三酯(triglycerides,TG)含量测定法评价其对3T3-L1前脂肪细胞分化的影响。采用RT-PCR法检测脂肪细胞中过氧化物酶体增殖体激活受体γ(peroxisome proliferators-activated receptors gamma,PPARγ)、CCAAT增强子结合蛋白α(CCAAT/enhancer bind-ing protein alpha,C/EBPα)、固醇调节元件结合蛋白-1c(ste-rol regulatory element binding protein-1c,SREBP-1c)等分化相关基因的mRNA表达水平。结果 AM-CHS能明显抑制3T3-L1前脂肪细胞和成熟脂肪细胞的增殖,抑制3T3-L1前脂肪细胞的分化过程,以对分化早期的抑制作用最强。RT-PCR结果表明,AM-CHS能明显降低脂肪细胞PPARγ、C/EBPα和SREBP-1c mRNA的表达。结论海地瓜AM-CHS能明显抑制3T3-L1前脂肪细胞的增殖和分化,其作用机制与下调分化相关基因PPARγ、C/EBPα和SREBP-1c的表达有关。     

催产素对3T3-L1脂肪细胞糖脂代谢的影响

目的 观察催产素对3T3-L1脂肪细胞糖脂代谢的影响。方法 3T3-L1前脂肪细胞体外培养,并诱导其分化成熟为脂肪细胞。研究催产素对脂肪细胞葡萄糖消耗量以及三酰甘油、游离脂肪酸和甘油的影响。采用实时荧光定量PCR法检测糖脂代谢相关基因GLUT-1、GLUT-4、ATGT、HSL的m RNA表达。结果 与对照组比较,催产素20、50、100μg/m L组葡萄糖消耗量有所增加,且表现出剂量相关。催产素组较对照组的三酰甘油降低,而甘油和游离脂肪酸增高。催产素50μg/m L组中脂代谢相关基因HSL表达明显高于对照组,糖代谢相关基因GLUT-4 m RNA表达水平增加。结论 催产素处理可减少3T3-L1细胞脂质合成、增加脂质分解作用,并可明显改善脂质积聚。     

板蓝根水提物对3T3-L1前脂肪细胞增殖和分化的影响

目的探讨板蓝根水提物(water extract of Radix Isatidis,WERI)对3T3-L1前脂肪细胞增殖分化的影响及其作用机制。方法体外培养3T3-L1前脂肪细胞,MTT法和流式细胞技术检测WERI对细胞增殖的影响;鸡尾酒诱导剂诱导3T3-L1前脂肪细胞,油红O染色和比色分析法观察WERI对前脂肪细胞分化及脂肪积累的影响;采用RT-PCR检测脂肪细胞的过氧化物酶体增殖物激活受体γ(peroxisome proliferator-activated receptorγ,PPARγ)及CCAAT/增强子结合蛋白α(CCAAT/enhancer-binding proteinα,C/EBPα)mRNA的表达;Western blot法检测PPARγ及C/EBPα蛋白表达。结果WERI在一定浓度范围内能有效抑制3T3-L1前脂肪细胞增殖,同时细胞周期呈现G_0/G_1向S期阻滞;与空白组相比,用不同浓度的WERI处理后,3T3-L1前脂肪细胞的分化受到明显抑制,且细胞内脂滴生成量明显减少;PCR及Western blot结果显示,WERI还可以抑制脂肪细胞PPARγ和C/EBPα基因及蛋白的表达。结论 WERI具有抑制3T3-L1前脂肪细胞增殖作用,并可通过下调PPARγ和C/EBPαmRNA及蛋白表达来抑制细胞成脂分化。     

MiR-24对3T3-L1脂肪细胞分化及脂肪型脂肪酸结合蛋白表达的调节作用

目的探讨microRNAs对脂肪细胞分化过程的调节作用分子机制及其对脂肪特异性基因——脂肪型脂肪酸结合蛋白(fatty acid binding protein,FABP4)表达的影响。方法用microRNAs微阵列分析法筛选和鉴定3T3-L1脂肪细胞分化相关性microRNAs,构建脂肪细胞分化相关性micro-RNAs的高表达质粒,通过脂质体介导转染3T3-L1前体脂肪细胞,观察脂肪相关性microRNAs对脂肪细胞分化过程的影响,Westernblot和RT-PCR分别检测FABP4蛋白及其mR-NA在脂肪细胞分化过程中的表达变化。结果3T3-L1脂肪细胞分化过程中microRNA表达谱发生明显改变,其中35个microRNAs下调,miR-24最明显;17个microRNAs上调,miR-21最明显;用不同脂肪相关性microRNAs转染3T3-L1前体脂肪细胞并高表达后,发现miR-24明显抑制脂肪细胞的分化与成熟,而miR-21则无影响;miR-24明显抑制FABP4蛋白表达,但对其mRNA无影响,miR-21对FABP4的蛋白和mRNA表达都没有影响。结论3T3-L1脂肪细胞分化过程中存在脂肪细胞分化相关性microRNAs;miR-24脂肪细胞分化过程及其脂肪特异蛋白FABP4表达有重要的调节作用。     

调血脂药对3T3-L1脂肪细胞脂肪水孔蛋白mRNA表达的影响

目的　通过细胞培养研究非诺贝特、洛伐他汀对成熟脂肪细胞脂肪水孔蛋白 (aquaporinadipose,AQPaP)基因表达的影响 ,了解调脂药对AQPaP基因表达有无影响 ,探讨其在肥胖及糖尿病发病中所起作用以及调脂药的药理作用机制。方法　以 10 0 μmol/L、2 5 0 μmol/L非诺贝特及 10 μmol/L洛伐他汀刺激诱导分化第 9天的 3T3 L1脂肪细胞 4 8h ,提取细胞RNA ,运用半定量反转录聚合酶链反应技术 ,检测AQPapmRNA表达量的变化。结果　 10 0 μmol/L非诺贝特刺激脂肪细胞 4 8h后 ,AQPapmRNA表达量有所增加 ,浓度升至 2 5 0 μmol/L ,AQPapmRNA表达量又有下降 ,但各组之间差异无显著性 (P >0 0 5 )。 10 μmol/L洛伐他汀刺激 3T3 L1脂肪细胞4 8h ,与对照组相比 ,AQPapmRNA表达量略有下降 ,但差异无显著性 (P >0 0 5 )。与非诺贝特刺激组相比差异也无显著性差异 (P >0 0 5 )。结论　非诺贝特对脂肪细胞AQPaP基因表达无直接作用。而洛伐他汀对AQPap基因表达也无影响 ,AQPap可能是过氧化物酶体增生剂激活受体 γ(PPAR γ)的一个下游基因     

Biflavones of Ginkgo biloba stimulate lipolysis in 3T3-L1 adipocytes

Ginkgo biloba L. biflavones were shown to increase cAMP phosphodiesterase activity and to stimulate skin microcirculation. The aim of this study was to investigate whether biflavones were able to stimulate lipolysis in adipocytes. Lipolysis was assayed in fully differentiated 3T3-L1 fat cells in the presence of biflavones at 0.005 - 100 microM. Cell viability was evaluated at 0.5 -100 microM. Theophylline and caffeine were used as reference compounds. Lipolytic activity in untreated cells was 0.62 +/- 0.15 micromoles glycerol/mg DNA/h. All biflavones except sciadopitysin stimulated lipolysis in a concentration-dependent fashion. Maximal stimulation was observed at 0.1 - 0.5 microM. At higher concentrations the effect diminished progressively and was lost at 100 microM. Only a partial loss of cell viability was observed with biflavones at 10 - 100 microM.     

Berberine activates GLUT1-mediated glucose uptake in 3T3-L1 adipocytes

It has recently been known that berberine, an alkaloid of medicinal plants, has anti-hyperglycemic effects. To explore the mechanism underlying this effect, we used 3T3-L1 adipocytes for analyzing the signaling pathways that contribute to glucose transport. Treatment of berberine to 3T3-L1 adipocytes for 6 h enhanced basal glucose uptake both in normal and in insulin-resistant state, but the insulin-stimulated glucose uptake was not augmented significantly. Inhibition of phosphatidylinositol 3-kinase (PI 3-K) by wortmannin did not affect the berberine effect on basal glucose uptake. Berberine did not augment tyrosine phosphorylation of insulin receptor (IR) and insulin receptor substrate (IRS)-1. Further, berberine had no effect on the activity of the insulin-sensitive downstream kinase, atypical protein kinase C (PKCzeta/lambda). However, interestingly, extracellular signal-regulated kinases (ERKs), which have been known to be responsible for the expression of glucose transporter (GLUT)1, were significantly activated in berberine-treated 3T3-L1 cells. As expected, the level of GLUT1 protein was increased both in normal and insulin-resistant cells in response to berberine. But berberine affected the expression of GLUT4 neither in normal nor in insulin-resistant cells. In addition, berberine treatment increased AMP-activated protein kinase (AMPK) activity in 3T3-L1 cells, which has been reported to be associated with GLUT1-mediated glucose uptake. Together, we concluded that berberine increases glucose transport activity of 3T3-L1 adipocytes by enhancing GLUT1 expression and also stimulates the GLUT1-mediated glucose uptake by activating GLUT1, a result of AMPK stimulation.     

Effects of leptin on apoptosis and adipogenesis in 3T3-L1 adipocytes

Leptin has been demonstrated to induce adipose tissue apoptosis, which can contribute to the decrease of adiposity, after either central nervous system or peripheral administration. However, it is not known whether leptin acts only centrally to initiate a signal or can also act directly on adipocytes to induce apoptosis. The objective of this study was to determine the direct effect of leptin on adipocyte apoptosis and adipogenesis in vitro using 3T3-L1 cell lines. An ELISA for single stranded DNA, which is highly specific for apoptotic cells, was used to quantify apoptosis. Preconfluent preadipocytes treated with 10(-9), 10(-8), 10(-7), and 10(-6)M leptin showed inhibitory effects on cell viability, and similar observations were also found in maturing preadipocytes treated during day 0-2 and day 2-4 of maturation. After 48 h incubation with 10(-6)M leptin, LDH release was increased by 24.3% (p<0.05) in preconfluent preadipocytes and by 108.5% (p<0.01) in maturing preadipocytes. However, ssDNA analysis revealed no increased apoptosis in preconfluent or maturing preadipocytes or in mature adipocytes treated with leptin. Leptin significantly reduced lipid accumulation and GPDH activity in maturing preadipocytes, demonstrating an inhibitory effect of leptin on adipogenesis. These results indicate that leptin does not act directly to induce adipocyte apoptosis, but can act directly to inhibit maturation of preadipocytes.     

Vanadium and insulin increase adiponectin production in 3T3-L1 adipocytes.

Both adiponectin, an adipokine secreted by adipocytes, and vanadium compounds, have been extensively shown to enhance insulin sensitivity in vivo and in vitro. In this study we examined whether insulin and vanadyl sulfate (VS) affected adiponectin release and cell content from 3T3-L1 adipocytes, and whether they acted through a similar signaling pathway. Adiponectin cell content, but not release, consistently increased in cells treated with insulin (100 nM) and VS (10 and 50 microM) after 24 h. On the other hand, VS-induced adiponectin release only occurred after 4 days of incubation. The protein kinase B (PKB) inhibitor, NL-71-101, decreased both insulin and VS-induced adiponectin cell content, while neither wortmannin nor LY 294002, inhibitors of phosphatidylinositol 3-kinase (PI3-K), attenuated insulin or VS-induced adiponectin cell content. Furthermore, VS-induced adiponectin accumulation occurred in the presence of AGL2263, an insulin receptor (IR) inhibitor. These studies provide the first evidence that vanadium could exert its insulin sensitizing effects through the stimulation of adiponectin through a PKB-dependent transduction pathway.     

Evodiamine activates AMPK and promotes adiponectin multimerization in 3T3-L1 adipocytes

Adiponectin, an adipokine with insulin-sensitizing effect, is secreted from adipocytes into circulation as high, medium, and low molecular weight (HMW, MMW, and LMW) forms. The HMW adiponectin is more metabolically active and the ratio of HMW adiponectin to total adiponectin directly correlates with insulin sensitivity. Evodiamine is an indole alkaloid found in the traditional Chinese medicinal plant Evodia rutaecarpa. In this study, evodiamine was found to activate AMP-activated protein kinase (AMPK) in both 3T3-L1 adipocytes and 293T cells. Activation of AMPK by evodiamine promoted the assembly of HMW adiponectin and increased the HMW/total ratio of adiponectin in 3T3-L1 adipocytes. The Ca²⁺-dependent PI3K/Akt/CaMKII-signaling pathway was demonstrated to be involved in evodiamine-induced AMPK activation. This study revealed a novel role of this Ca²⁺-mediated signaling pathway in promoting the multimerization of adiponectin.     

Antidiabetic agent pioglitazone increases insulin receptors on 3T3-L1 adipocytes

Pioglitazone and other antidiabetic thiazolidinediones appear to overcome insulin resistance by affecting an unidentified early event in insulin action. Because attempts to determine changes in insulin receptors in tissues from thiazolidinedione-treated diabetic animals are complicated by drug-induced reduction of hyperinsulinemia and consequent receptor up-regulation, 3T3-L1 cells were utilized here as an in vitro model system. After the excess insulin required for optimal differentiation of 3T3-L1 adipocytes was removed from the culture medium, there was an increase in specific binding of insulin to the cell surface that was further augmented 25 and 47% in cells treated with pioglitazone for 12 and 24 h, respectively (EC₅₀ about 0.6 μM, maximal at 5–25 μM). Pioglitazone increased the number of insulin receptors without changing binding affinity. Specific IGF-I binding was not affected by pioglitazone in the 3T3-L1 cells. Glycerol 3-phosphate dehydrogenase activity, a marker of adipocyte differentiation, was also increased in a dose-dependent manner by pioglitazone (maximal at 10–25 μM). Tunicamycin, which inhibits the N-linked glycosylation of newly synthesized insulin receptors that is required for their translocation to the cell surface, decreased specific insulin binding by about 50% after 24 h, and this decrease remained unchanged when pioglitazone was simultaneously present. Pioglitazone increased not only cell surface insulin receptors, but also total cellular insulin receptors (quantitated either by specific insulin binding or by immunoblotting) and insulin receptors mRNA. In addition, among several structurally related thiazolidinediones there was a positive correlation between in vivo antihyperglycemic activity and their ability to increase insulin binding in vitro, suggesting a possible common molecular mechanism for these actions. © 1995 Wiley-Liss, Inc.     

促甲状腺激素对3T3-L1脂肪细胞葡萄糖转运蛋白4表达的影响

目的 探讨促甲状腺激素(TSH)对3T3-L1脂肪细胞葡萄糖转运蛋白4(GLUT4)表达的影响.方法 体外诱导3T3-L1前脂肪细胞为成熟脂肪细胞.以不同浓度牛TSH(0.01 IU/L、0.1 IU/L、1 IU/L)刺激成熟脂肪细胞,蛋白质印迹法分别检测48 h后成熟脂肪细胞GLUT4蛋白表达水平,ELISA方法检测细胞培养液中自细胞介素6(IL-6)水平.结果 与空白对照组相比,以不同浓度(0.01、0.1、1 IU/L)牛TSH刺激成熟脂肪细胞48 h后GLUT4蛋白表达呈下降趋势,分别下降约23%、44%、74%(均P<0.05),细胞培养液中IL-6水平明显增加[(101.9300±6.8396)、(104.1533±5.9619)、(129.0167±6.4232)比/L比(93.2500±2.6695)μg/L,P<0.05].结论 TSH可下调3T3-L1脂肪细胞GLUT4蛋白的表达.

Abstract：

Objective To test if thyroid-stimulating hormone(TSH) can suppress expression of glucose transporter 4(GLUT4)in 3T3-L1 adipocytes. Methods 3T3-L1 preadipocytes were induced to differentiate into adipocytes. These adipocytes were treated with 0 to 1.0 IU/L TSH for up to 48 hours. Protein levels of total GLUT4 were quantified by western blotting. Culture medium interleukin-6 level was assessed by enzyme-linked immunosor-bent assay(ELI(S)A). Results The GLUT4 protein level after 48 hours induced with different dose(0. 01 IU/L, 0.1 IU/L, 1 IU/L) of TSH presented a significant 23% , 44% , 74% ( all P < 0.05 ) reduction compared with control group. While the interleukin-6 level of culture medium increased significantly [( 101. 9300 ± 6. 8396), (104.1533 ±5.9619), (129.0167 ±6.4232) μg/L vs (93.2500 ±2.6695)μg/L, P<0.05]. Conclusion In 3T3-L1 adipocytes, TSH can decrease expression of GLUT43.     

脂肪因子Apelin-13对3T3-L1脂肪细胞水通道蛋白7基因表达的影响

目的 探讨脂肪因子Apelin-13对3T3-L1脂肪细胞水通道蛋白7（AQP7）基因表达的影响.方法 体外培养3T3-L1脂肪细胞,以油红O染色鉴定为成熟脂肪细胞后,分为阴性对照组（无干预）,不同浓度（10^-9、10^-8、10^-7、10^-6nmol/L） Apelin-13干预组（均干预24 h）,阳性对照组（10^-5 nmol/L罗格列酮干预24 h）和10^-7 nmol/L Apelin-13干预不同时间（0、12、24、36、48 h）组.用反转录-聚合酶链反应检测各组细胞AQP7 mRNA表达水平.结果 阴性对照组、10^-9、10^-8、10^-7、10^-6 nmol/L Apelin-13和阳性对照组AQP7表达水平分别为（0.22±0.02）、（0.29±0.07）、（0.36±0.05）、（0.43±0.05）、（0.31±0.06）、（0.32±0.08）,阳性对照组与阴性对照组之间差异有统计学意义（P＜0.05）;与阴性对照组比较,10^-8、10^-7 nmol/L Apelin-13能明显刺激AQP7 mRNA表达（P ＜0.05）;10^-8、10^-7 nmol/L Apelin-13组与阳性对照组比较,10^-7 nmol/L Apelin-13能明显刺激AQP7 mRNA表达（P＜0.05）;10^-8、10^-7 nmol/L Apelin-13组间差异无统计学意义.在时间组中,10^-7 nmol/L Apelin-13的0、12、24、36、48 h各组灰度比值分别为（0.27±0.09）、（0.43±0.07）、（0.55±0.10）、（0.42±0.08）、（0.33±0.09）,12、24、36 h组AQP7 mRNA表达较0h组能明显刺激AQP7 mRNA表达（P＜0.05）,作用24 h表达最高;但12、24、36h3组之间AQP7mRNA表达差异无统计学意义.结论 Apelin-13在一定程度上能增加3T3-L1脂肪细胞AQP7 mRNA表达的水平,并分别以10^-7 nmol/L和24 h为最佳作用浓度和时间.