It has recently become clear that obstructive sleep apnea (OSA) is an independent risk factor for the development of metabolic syndrome, a disorder of defective energy storage and use. Several mechanisms have been proposed to explain this finding, drawing upon the characteristics that define OSA. In particular, intermittent hypoxia, sleep fragmentation, elevated sympathetic tone, and oxidative stress — all consequences of OSA — have been implicated in the progression of poor metabolic outcomes in OSA. In this review we examine the evidence to support each of these disease manifestations of OSA as a unique risk for metabolic dysfunction. Tissue hypoxia and sleep fragmentation are each directly connected to insulin resistance and hypertension, and each of these also may increase sympathetic tone, resulting in defective glucose homeostasis, excessive lipolysis, and elevated blood pressure. Oxidative stress further worsens insulin resistance and in turn, metabolic dysfunction also increases oxidative stress. However, despite many studies linking each of these individual components of OSA to the development of metabolic syndrome, there are very few reports that actually provide a coherent narrative about the mechanism underlying metabolic dysfunction in OSA.

中文翻译：

---

阻塞性睡眠呼吸暂停的代谢功能障碍：对潜在机制的批判性检查

最近已经明确，阻塞性睡眠呼吸暂停 (OSA) 是代谢综合征（一种能量储存和使用缺陷的疾病）发展的独立危险因素。已经提出了几种机制来解释这一发现，利用定义 OSA 的特征。特别是，间歇性缺氧、睡眠碎片化、交感神经张力升高和氧化应激——所有 OSA 的后果——都与 OSA 代谢不良结果的进展有关。在这篇综述中，我们检查了支持 OSA 的每一种疾病表现作为代谢功能障碍的独特风险的证据。组织缺氧和睡眠碎片化均与胰岛素抵抗和高血压直接相关，并且每一种都可能增加交感神经张力，导致葡萄糖稳态缺陷，过度的脂肪分解和血压升高。氧化应激会进一步恶化胰岛素抵抗，反过来，代谢功能障碍也会增加氧化应激。然而，尽管许多研究将 OSA 的这些单独组成部分与代谢综合征的发展联系起来，但很少有报告实际上提供了关于 OSA 代谢功能障碍潜在机制的连贯叙述。