睡眠呼吸暂停：脂毒性的一个被忽视的原因？
Sleep apnea: An overlooked cause of lipotoxicity?
机构信息
Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA; Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Division of Pulmonary and Critical Care, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA.
出版信息
Med Hypotheses. 2017 Oct;108:161-165. doi: 10.1016/j.mehy.2017.09.007. Epub 2017 Sep 13.
Obstructive sleep apnea (OSA) is a common sleep disorder associated with diabetes and cardiovascular disease. However, the mechanisms by which OSA causes cardiometabolic dysfunction are not fully elucidated. OSA increases plasma free fatty acids (FFA) during sleep, reflecting excessive adipose tissue lipolysis. In animal studies, intermittent hypoxia simulating OSA also increases FFA, and the increase is attenuated by beta-adrenergic blockade. In other contexts, excessive plasma FFA can lead to ectopic fat accumulation, insulin resistance, vascular dysfunction, and dyslipidemia. Herein, we propose that OSA is a cause of excessive adipose tissue lipolysis contributing towards systemic "lipotoxicity". Since visceral and upper-body obesity contributes to OSA pathogenesis, OSA-induced lipolysis may further aggravate the consequences of this metabolically harmful state. If this hypothesis is correct, then OSA may represent a reversible risk factor for cardio-metabolic dysfunction, and this risk might be mitigated by preventing OSA-induced lipolysis during sleep.
阻塞性睡眠呼吸暂停（OSA）是一种常见的睡眠障碍，与糖尿病和心血管疾病有关。然而，OSA 导致心脏代谢功能障碍的机制尚未完全阐明。OSA 在睡眠期间会增加血浆游离脂肪酸（FFA），反映出脂肪组织过度脂解。在动物研究中，模拟 OSA 的间歇性缺氧也会增加 FFA，而β-肾上腺素能阻断可减轻这种增加。在其他情况下，过多的血浆 FFA 会导致异位脂肪堆积、胰岛素抵抗、血管功能障碍和血脂异常。在此，我们提出 OSA 是导致全身“脂毒性”的脂肪组织过度脂解的原因。由于内脏和上身肥胖有助于 OSA 的发病机制，OSA 诱导的脂解可能会进一步加重这种代谢有害状态的后果。如果这一假设是正确的，那么 OSA 可能是心脏代谢功能障碍的可逆危险因素，通过在睡眠期间防止 OSA 诱导的脂解，可以减轻这种风险。
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