Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis:: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers
Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis:: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers
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DOI：
10.1016/j.cyto.2005.08.003
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发表时间：
2005-10-21
期刊：
影响因子：
3.8
通讯作者：
Boon, L
中科院分区：
文献类型：
--
作者：
Simons, PJ;van den Pangaart, PS;Boon, L
在过去的十年中，令人信服的证据已经提出，细胞因子影响脂肪细胞组织的形成和功能。在本研究中，我们探讨了促炎因子(即白细胞介素(IL)-1 β、IL-6、干扰素（IFN)- γ和肿瘤坏死因子(TNF)- α）与抗炎因子(即IL-4、IL-10和转化生长因子（TGF)- β(1)）在体外人脂肪形成过程中对瘦素和脂联素分泌的影响。证实先前的报道，暴露于tnf - α、IL-1 β、ifn - γ或tgf - β后，前体前脂肪细胞向成熟脂肪细胞的转化被完全抑制(1)。因此，所有这些抗脂肪生成细胞因子阻止了脂肪细胞特异性脂联素的释放。ifn - γ也能显著降低瘦素的产生（>= 85%）。然而，在没有成熟脂肪细胞的情况下，tnf - α、IL-1 β和tgf - β(1)刺激脂肪前细胞产生瘦素（分别为20.6 +/- 5.4 ng/ml、100.8 +/- 18.2 ng/ml和5.4 +/- 0.4 ng/ml，而对照组脂肪细胞培养在第21天为6.6 +/- 0.8 ng/ml; n = 4）。IL-4、IL-6和IL-10对脂肪细胞分化及其激素分泌没有或仅有轻微影响。综上所述，脂联素和瘦素都是由脂肪细胞合成的，而瘦素也由脂肪前细胞在tnf - α或IL-1 β刺激下产生。这些数据表明，前脂肪细胞对总循环瘦素水平的贡献可能比之前认为的要大，特别是在患病的情况下，这些促炎因子发挥了突出的作用。(c) 2005 Elsevier Ltd版权所有。
Over the last decade, compelling evidence has been presented that cytokines affect adipocyte tissue formation and function. In this study we explored the effect of pro-inflammatory (i.e. interleukin (IL)-1 beta, IL-6, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha) versus anti-inflammatory cytokines (i.e. IL-4, IL-10, and transforming growth factor (TGF)-beta(1)) on leptin and adiponectin secretion during in vitro human adipogenesis. Confirmative to previous reports, conversion of precursor preadipocytes into mature adipocytes was completely inhibited upon exposure to TNF-alpha, IL-1 beta, IFN-gamma, or TGF-beta(1). Hence, all these anti-adipogenic cytokines prevented release of adipocyte-specific adiponectin. IFN-gamma also strongly reduced leptin production (>= 85%). However, TNF-alpha, IL-1 beta, and TGF-beta(1) stimulated leptin production from preadipocytes in the absence of mature adipocytes (20.6 +/- 5.4 ng/ml, 100.8 +/- 18.2 ng/ml, and 5.4 +/- 0.4 ng/ml, respectively, compared to 6.6 +/- 0.8 ng/ml in control adipocyte cultures on day 2 1; n = 4). IL-4, IL-6 and IL-10 did not, or only slightly, affect adipocyte differentiation and their hormonal secretion. In conclusion, adiponectin and leptin are both synthesized by adipocytes, whereas leptin is also produced by preadipocytes upon TNF-alpha or IL-1 beta stimulation. These data suggest that preadipocytes could contribute more to total circulating leptin levels than has been previously considered, especially in diseased conditions were these pro-inflammatory factors play a prominent role. (c) 2005 Elsevier Ltd. All rights reserved.