Recently, Murphy et al. [1] demonstrated, through a challenging animal, cellular and human translational approach, that intermittent hypoxia induces a pro-inflammatory activation of adipose tissue macrophages (ATMs), promoting insulin resistance. They confirmed that intermittent hypoxia lowers insulin-mediated glucose uptake in 3T3-L1 adipocytes, and evidenced the interrelationship between inflammation and insulin resistance in the adipose tissue of mice exposed to intermittent hypoxia. They then measured the concentration of serum soluble CD163 (sCD163), an assumed pro-inflammatory biomarker reflecting macrophage activation, in obstructive sleep apnoea (OSA) patients classified according to their BMI and apnoea/hypopnoea index (AHI). This is the first time serum sCD163 has been evaluated in OSA patients, and its association with AHI is promising. With the aim of enhancing its relevance in further studies, we wish to discuss the following points. Serum sCD163 as a biomarker of adipose tissue inflammation in OSA patients: limits and perspectives http://ow.ly/kgxL30d7RnE

中文翻译：

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血清 sCD163 作为阻塞性睡眠呼吸暂停患者脂肪组织炎症的生物标志物：局限性和前景

最近，墨菲等人。[1] 通过具有挑战性的动物、细胞和人类转化方法证明，间歇性缺氧会诱导脂肪组织巨噬细胞 (ATM) 的促炎性激活，从而促进胰岛素抵抗。他们证实，间歇性缺氧会降低 3T3-L1 脂肪细胞中胰岛素介导的葡萄糖摄取，并证明了暴露于间歇性缺氧的小鼠脂肪组织中炎症与胰岛素抵抗之间的相互关系。然后，他们测量了根据 BMI 和呼吸暂停/低通气指数 (AHI) 分类的阻塞性睡眠呼吸暂停 (OSA) 患者中血清可溶性 CD163 (sCD163) 的浓度，这是一种反映巨噬细胞激活的假定促炎生物标志物。这是首次在 OSA 患者中评估血清 sCD163，它与 AHI 的关联是有希望的。为了增强其在进一步研究中的相关性，我们希望讨论以下几点。血清 sCD163 作为 OSA 患者脂肪组织炎症的生物标志物：局限性和前景 http://ow.ly/kgxL30d7RnE