High fat intake induces a population of adipocytes to co-express TLR2 and TNFα in mice with insulin resistance
High fat intake induces a population of adipocytes to co-express TLR2 and TNFα in mice with insulin resistance
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DOI：
10.1016/j.bbrc.2007.01.039
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发表时间：
2007-03-16
影响因子：
3.1
通讯作者：
Saito, Yasushi
中科院分区：
文献类型：
--
作者：
Murakami, Kentaro;Bujo, Hideaki;Saito, Yasushi
脂肪组织中细胞因子的产生在胰岛素抵抗中起关键作用。本研究的目的是了解高脂诱导胰岛素抵抗脂肪细胞表型的变化。高脂肪摄入诱导内脏脂肪组织中肿瘤坏死因子α（TNF α）的表达以及胰岛素抵抗的发展。对脂肪细胞中基因表达谱的分析表明，高脂肪摄入除了诱导TNFa外，还诱导了Toll样受体2（TLR 2）的表达。流式细胞术分析显示存在共表达TLR 2和TNF α的脂肪细胞（TLR 2/TNF α-脂肪细胞），并且与皮下脂肪组织相比，内脏脂肪组织中的TLR 2/TNF α-脂肪细胞的数量通过高脂肪摄入而增加。游离脂肪酸通过TLR 2信号增加3 T3-L1脂肪细胞中TNF α的表达。这些结果表明，TLR 2/TNF α-脂肪细胞可能引起内脏脂肪组织中TNF α表达的诱导，与高脂肪诱导的胰岛素抵抗的发展相关。(c)2007年爱思唯尔公司All rights reserved.
Cytokine production in fat tissue plays a key role in insulin resistance. The aim of study is to know the phenotypic changes of adipocytes with high fat-induced insulin resistance. High fat intake induced the expression of tumor necrosis factor alpha (TNF alpha) in visceral fat tissue as well as development of insulin resistance. Analysis of the gene expression profiles in adipocytes showed that high fat intake induced the expression of toll-like receptor 2 (TLR2) in addition to TNFa. Flow cytometry analysis revealed the presence of adipocytes co-expressing TLR2 and TNF alpha (TLR2/TNF alpha-adipocytes), and the number of TLR2/TNF alpha-adipocytes in visceral fat tissues was increased by high fat intake compared to that in subcutaneous fat tissues. Free fatty acids increased TNF alpha expression in 3T3-L1 adipocytes through TLR2 signals. These results indicate that TLR2/TNFa-adipocytes possibly cause the induction of TNF alpha expression in visceral fat tissues, being associated with the development of high fat-induced insulin resistance. (c) 2007 Elsevier Inc. All rights reserved.