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瘦素在阻塞性睡眠呼吸暂停中的作用。

Role of Leptin in Obstructive Sleep Apnea.

机构信息

Division of Pulmonary, Critical Care, Sleep, and Allergy, College of Medicine, University of Illinois at Chicago, Chicago, Illinois; and Jesse Brown VA Medical Center, Chicago, Illinois.

出版信息

Ann Am Thorac Soc. 2017 Nov;14(11):1607-1621. doi: 10.1513/AnnalsATS.201702-181FR.

DOI:10.1513/AnnalsATS.201702-181FR
PMID:28796527
Abstract

Leptin is a peptide hormone produced mainly in white adipose tissue. It is known to regulate energy homeostasis, inflammation, metabolism, and sympathetic nerve activity. Increasing evidence suggests it has a role in ventilatory function and upper airway obstruction. Leptin levels correlate positively with measurements of adiposity and can potentially provide important insights into the pathophysiology of diseases associated with obesity. Obesity is a strong risk factor for obstructive sleep apnea, a disease characterized by periodic upper airway occlusion during sleep. The neuromuscular activity that maintains upper airway patency during sleep and the anatomy of upper airway are key factors involved in its pathogenesis. Experimental studies using animal models of a low leptin state such as leptin deficiency have shown that leptin regulates sleep architecture, upper airway patency, ventilatory function, and hypercapnic ventilatory response. However, findings from human studies do not consistently support the data from the animal models. The effect of leptin on the pathophysiology of obstructive sleep apnea is being investigated, but the results of studies have been confounded by leptin's diurnal variation and the short-term effects of feeding, adiposity, age, and sex. Improved study design and methods of assessing functional leptin levels, specifically their central versus peripheral effects, will improve understanding of the role of leptin in sleep apnea.

摘要

瘦素是一种主要在白色脂肪组织中产生的肽类激素。它已知可以调节能量平衡、炎症、代谢和交感神经活性。越来越多的证据表明它在通气功能和上气道阻塞中发挥作用。瘦素水平与肥胖的测量值呈正相关,并且可以为与肥胖相关的疾病的病理生理学提供重要的见解。肥胖是阻塞性睡眠呼吸暂停的强烈危险因素,这种疾病的特征是睡眠期间上气道周期性阻塞。维持睡眠中上气道通畅的神经肌肉活动和上气道解剖结构是其发病机制中的关键因素。使用瘦素缺乏等低瘦素状态的动物模型进行的实验研究表明,瘦素调节睡眠结构、上气道通畅性、通气功能和高碳酸血症通气反应。然而,来自人体研究的结果并不一致支持动物模型的数据。瘦素对阻塞性睡眠呼吸暂停病理生理学的影响正在研究中,但研究结果受到瘦素的昼夜变化以及短期喂养、肥胖、年龄和性别的影响。改善研究设计和评估功能性瘦素水平的方法,特别是其中枢和外周作用,将提高对瘦素在睡眠呼吸暂停中的作用的理解。

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