Preadipocyte response and impairment of differentiation in an inflammatory environment
Preadipocyte response and impairment of differentiation in an inflammatory environment
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DOI：
10.1016/j.bbrc.2007.03.053
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发表时间：
2007-05-11
影响因子：
3.1
通讯作者：
Froguel, Philippe
中科院分区：
文献类型：
--
作者：
Poulain-Godefroy, Odile;Froguel, Philippe
最近的研究表明，Toll样受体4（TLR 4）在炎症反应和脂肪酸诱导的胰岛素抵抗的启动中具有潜在的作用。我们在这里描述的3 T3-L1前脂肪细胞系中的促炎性产物的合成与脂多糖（LPS），TLR 4激动剂刺激后。编码IL 6、CCL 2、CCL 5、CCL 11、NOS 2和PTGS 2的mRNA的表达谱表明，前脂肪细胞中这些转录物对LPS的反应性高于完全分化的脂肪细胞，证实了前脂肪细胞的炎症特征。LPS刺激后4 h内3 T3-L1细胞培养上清分泌IL 6、CCL 2、CCL 5和CCL 11。此外，在脂肪细胞分化过程中连续暴露于LPS损害了这一过程，如通过分析脂肪生成酶（FABP 4、GPD 1、LPL）、脂肪因子（脂联素、内脂素、瘦素）和转录因子PPAR γ的mRNA谱所证明的。这表明，Toll样受体介导的活化可以调节前脂肪细胞状态的维持，以及发炎的白色脂肪组织中遇到的炎症环境。(c)2007爱思唯尔公司All rights reserved.
Recent reports suggest the potential role of toll-like receptor 4 (TLR4) in initiation of inflammatory responses and fatty acid-induced insulin resistance. We describe here the synthesis of pro-inflammatory products in 3T3-L1 preadipocyte cell line after stimulation with lipopolysaccharide (LPS), a TLR4 agonist. Expression profiles of mRNA coding for IL6, CCL2, CCL5, CCL11, NOS2, and PTGS2 demonstrated a higher responsiveness to LPS of these transcripts in preadipocytes than in fully differentiated adipocytes, confirming inflammatory features of preadipocytes. IL6, CCL2, CCL5 and CCL11 were secreted in 3T3-L1 supernatants within 4 h after LPS stimulation. In addition, continuous exposure to LPS during adipocyte differentiation impaired this process as was demonstrated by analysis of mRNA profiles of lipogenesis enzymes (FABP4, GPD1, LPL), adipokines (adiponectin, resistin, visfatin, leptin), and of the transcription factor PPAR gamma. This suggests that toll-like receptor mediated activation could regulate maintenance of preadipocyte status, and inflammatory environment encountered in inflamed white adipose tissue. (c) 2007 Elsevier Inc. All rights reserved.