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Peripheral IL-6/STAT3 signaling promotes beiging of white fat
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research ( IF 4.6 ) Pub Date : 2021-06-24 , DOI: 10.1016/j.bbamcr.2021.119080
Haifang Li 1 , Mei Dong 1 , Wenhui Liu 1 , Cheng Gao 1 , Yanxin Jia 1 , Xinzhi Zhang 1 , Xue Xiao 1 , Qingxin Liu 1 , Hai Lin 2
Affiliation  

Interleukin-6 (IL-6) can reportedly centrally affect the thermogenesis of brown fat. However, whether the peripheral IL-6 signaling regulates beiging of white fat remains largely unknown. In vitro experiments indicated IL-6-KO-derived white adipocytes exhibited lower thermogenic gene expression compared to the WT, associating with reduced phosphorylation of STAT3 at Tyr705. Mechanistically, exogenous IL-6 application increased the p-STAT3Tyr705 level, thus the phosphorylated STAT3 bound to the promoter regions, and enhanced the transcription of Pparγ and Ucp1. The protein interaction of PGC-1α with PPARγ was increased by IL-6, which also contributed to stimulate Ucp1 expression. In vivo experiments demonstrated that IL-6 KO decreased the beiging potential of white fat with suppressed STAT3 Tyr705 phosphorylation. Accordingly, IL-6-KO mature mice were associated with disrupted glucose homeostasis and accelerated hepatic steatosis. Collectively, we identified a novel function of peripheral IL-6/STAT3 signaling which is essential for beiging of white fat, such ensuring fat and glucose homeostasis.



中文翻译:

外周 IL-6/STAT3 信号促进白色脂肪变褐

据报道,白细胞介素 6 (IL-6) 可以集中影响棕色脂肪的产热。然而,外周 IL-6 信号是否调节白色脂肪的褐变仍然很大程度上未知。体外实验表明,与 WT 相比,IL-6-KO 衍生的白色脂肪细胞表现出较低的产热基因表达,这与 Tyr705 处 STAT3 的磷酸化降低有关。从机制上讲,外源性 IL-6 应用增加了 p-STAT3 Tyr705水平,因此磷酸化的 STAT3 与启动子区域结合,并增强了PparγUcp1的转录。IL-6 增加了 PGC-1α 与 PPARγ 的蛋白质相互作用,这也有助于刺激Ucp1表达。体内实验表明,IL-6 KO 降低了白色脂肪的褐变潜力,并抑制了 STAT3 Tyr705 磷酸化。因此,IL-6-KO 成熟小鼠与葡萄糖稳态破坏和肝脂肪变性加速有关。总的来说,我们确定了外周 IL-6/STAT3 信号传导的新功能,这对于白色脂肪的形成至关重要,例如确保脂肪和葡萄糖的稳态。

更新日期:2021-06-28
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