Inhibition of toll-like receptor 2 expression improves insulin sensitivity and signaling in muscle and white adipose tissue of mice fed a high-fat diet
Inhibition of toll-like receptor 2 expression improves insulin sensitivity and signaling in muscle and white adipose tissue of mice fed a high-fat diet
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DOI：
10.1677/joe-08-0354
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发表时间：
2008-12-01
影响因子：
4
通讯作者：
Saad, Mario J. A.
中科院分区：
文献类型：
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作者：
Caricilli, Andrea M.;Nascimento, Paula H.;Saad, Mario J. A.
本研究的目的是研究饮食诱导肥胖（DIO）小鼠肌肉和白色脂肪组织（WAT）中Toll样受体2（TLR2）的表达，以及使用TLR2反义寡核苷酸（ASON）抑制其对胰岛素敏感性和信号传导的影响。DIO小鼠肌肉和白色脂肪组织（WAT）中TLR2的表达增加， 与那些接受标准食物的人相比。通过 TLR2 ASON 抑制 DIO 小鼠中的 TLR2，改善了肌肉和 WAT 中的胰岛素和信号传导。此外，数据显示，抑制 TLR2 表达可阻止 DIO 小鼠中 IKBKB、MAPK8 和 IRS1 丝氨酸磷酸化的激活，表明 TLR2 是炎症和代谢途径之间串扰的关键调节剂。因此，我们建议选择性干扰 TLR2 为治疗肥胖和 2 型糖尿病的胰岛素抵抗提供了一个有吸引力的机会。
The aims of the present study were to investigate the expression of toll-like receptor-2 (TLR2) in muscle and white adipose tissue (WAT) of diet-induced obesity (DIO) mice, and also the effects of its inhibition, with the use of TLR2 antisense oligonucleotide (ASON), on insulin sensitivity and signaling, The expression of TLR2 was increased in muscle and WAT of DIO mice, compared with those that received standard chow. Inhibition of TLR2 in DIO mice, by TLR2 ASON, improved insulin and signaling in muscle and WAT In addition, data show that the inhibition of TLR2 expression prevents the activation of IKBKB, MAPK8, and serine phosphorylation of IRS1 in DIO mice, suggesting that TLR2 is a key modulator of the crosstalk between inflammatory and metabolic pathways. We, therefore, suggest chat a selective interference with TLR2 presents an attractive opportunity for the treatment of insulin resistance in obesity and type 2 diabetes.