在胰岛素抵抗小鼠中，高脂肪摄入会诱导一群脂肪细胞共表达Toll样受体2（TLR2）和肿瘤坏死因子α（TNFα）。
High fat intake induces a population of adipocytes to co-express TLR2 and TNFalpha in mice with insulin resistance.
作者信息
Murakami Kentaro, Bujo Hideaki, Unoki Hiroyuki, Saito Yasushi
机构信息
Department of Clinical Cell Biology, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
出版信息
Biochem Biophys Res Commun. 2007 Mar 16;354(3):727-34. doi: 10.1016/j.bbrc.2007.01.039. Epub 2007 Jan 17.
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 (TNFalpha) 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 TNFalpha. Flow cytometry analysis revealed the presence of adipocytes co-expressing TLR2 and TNFalpha (TLR2/TNFalpha-adipocytes), and the number of TLR2/TNFalpha-adipocytes in visceral fat tissues was increased by high fat intake compared to that in subcutaneous fat tissues. Free fatty acids increased TNFalpha expression in 3T3-L1 adipocytes through TLR2 signals. These results indicate that TLR2/TNFalpha-adipocytes possibly cause the induction of TNFalpha expression in visceral fat tissues, being associated with the development of high fat-induced insulin resistance.
脂肪组织中的细胞因子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肪诱导的胰岛素抵抗状态下脂肪细胞的表型变化。高脂肪摄入诱导内脏脂肪组织中肿瘤坏死因子α（TNFα）的表达以及胰岛素抵抗的发展。对脂肪细胞基因表达谱的分析表明，高脂肪摄入除了诱导TNFα表达外，还诱导Toll样受体2（TLR2）的表达。流式细胞术分析显示存在共表达TLR2和TNFα的脂肪细胞（TLR2/TNFα-脂肪细胞），与皮下脂肪组织相比，高脂肪摄入使内脏脂肪组织中TLR2/TNFα-脂肪细胞的数量增加。游离脂肪酸通过TLR2信号增加3T3-L1脂肪细胞中TNFα的表达。这些结果表明，TLR2/TNFα-脂肪细胞可能导致内脏脂肪组织中TNFα表达的诱导，与高脂肪诱导的胰岛素抵抗的发展有关。
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