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首页> 外文期刊>Cell metabolism >Hematopoietic cell-specific deletion of toll-like receptor 4 ameliorates hepatic and adipose tissue insulin resistance in high-fat-fed mice.
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Hematopoietic cell-specific deletion of toll-like receptor 4 ameliorates hepatic and adipose tissue insulin resistance in high-fat-fed mice.

机译：Toll样受体4的造血细胞特异性缺失可改善高脂喂养小鼠的肝脏和脂肪组织胰岛素抵抗。

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摘要

Chronic low-grade inflammation, particularly in adipose tissue, is an important modulator of obesity-induced insulin resistance. The Toll-like receptor 4 (Tlr4) is a key initiator of inflammatory responses in macrophages. We performed bone marrow transplantation (BMT) of Tlr4lps-del or control C57Bl/10J donor cells into irradiated wild-type C57Bl6 recipient mice to generate hematopoietic cell-specific Tlr4 deletion mutant (BMT-Tlr4(-/-)) and control (BMT-WT) mice. After 16 weeks of a high-fat diet (HFD), BMT-WT mice developed obesity, hyperinsulinemia, glucose intolerance, and insulin resistance. In contrast, BMT-Tlr4(-/-) mice became obese but did not develop fasting hyperinsulinemia and had improved hepatic and adipose insulin sensitivity during euglycemic clamp studies, compared to HFD BMT-WT controls. HFD BMT-Tlr4(-/-) mice also showed markedly reduced adipose tissue inflammatory markers and macrophage content. In summary, our results indicate that Tlr4 signaling in hematopoietic-derived cells is important for the development of hepatic and adipose tissue insulin resistance in obese mice.
机译：慢性低度炎症，尤其是在脂肪组织中，是肥胖引起的胰岛素抵抗的重要调节剂。 Toll样受体4（Tlr4）是巨噬​​细胞中炎症反应的关键引发剂。我们进行了Tlr4lps-del或对照C57Bl / 10J供体细胞的骨髓移植（BMT）到受辐照的野生型C57Bl6受体小鼠中，以生成造血细胞特异性Tlr4缺失突变体（BMT-Tlr4（-/-））和对照（BMT -WT）小鼠。经过16周的高脂饮食（HFD），BMT-WT小鼠出现了肥胖，高胰岛素血症，葡萄糖耐受不良和胰岛素抵抗。相比之下，与HFD BMT-WT对照相比，BMT-Tlr4（-/-）小鼠变得肥胖，但并未出现空腹高胰岛素血症，并且在正常血糖钳夹研究中改善了肝脏和脂肪胰岛素敏感性。 HFD BMT-Tlr4（-/-）小鼠还显示出明显减少的脂肪组织炎症标志物和巨噬细胞含量。总之，我们的结果表明，Tlr4信号在造血来源的细胞中对肥胖小鼠肝和脂肪组织胰岛素抵抗的发展很重要。

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