Toll-like receptors, inflammation, metabolism and obesity
Toll-like receptors, inflammation, metabolism and obesity
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DOI：
10.3109/13813455.2011.562514
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发表时间：
2011-07-01
影响因子：
3
通讯作者：
Cuesta, Natalia
中科院分区：
文献类型：
--
作者：
Fresno, Manuel;Alvarez, Ruth;Cuesta, Natalia
肥胖在西方国家是一个非常普遍的健康问题，导致许多重要的疾病，如2型糖尿病和代谢综合征，现在被认为是一种炎症性慢性疾病。脂肪细胞不再被认为是储存脂肪的被动细胞，因为它们是肥胖期间炎症细胞因子的主要生产者。脂肪细胞和巨噬细胞具有许多共同的生物学特性，包括合成类似的调节炎症的分子。脂肪酸水平在肥胖中升高，并通过一种大多未知的机制诱导炎症途径，导致胰岛素和瘦素抵抗的发展。最近的研究表明，这些作用可能是通过toll样受体（TLR）的激活介导的。TLR信号通路可能有助于肥胖相关胰岛素抵抗的发展，因此代表了先天免疫和代谢之间的联系。在这里，我们总结了最近关于tlr在脂肪组织、肥胖和胰岛素抵抗中发挥重要作用的证据。
Obesity is a highly prevalent health problem in Western countries that leads to many important diseases such as type 2 diabetes and metabolic syndrome being now considered an inflammatory chronic disease. Adipocytes are no longer considered passive cells storing fat since they are major producers of inflammatory cytokines during obesity. Adipocytes and macrophages share many biological properties including the synthesis of similar molecules regulating inflammation. Fatty acid levels are elevated in obesity and induce inflammatory pathways by yet a mostly unknown mechanism, leading to the development of insulin and leptin resistance. Recent studies suggest that these effects could be mediated through the activation of toll-like receptors (TLR). TLR signalling pathways might contribute to the development of obesity-associated insulin resistance, thus representing a connection between innate immunity and metabolism. Here, we summarize the recent evidence for the important role that TLRs play in adipose tissue, obesity and insulin resistance.