阻塞性睡眠呼吸暂停相关血脂异常的病理生物学:以肝脏为重点。

ISRN cardiology Pub Date : 2013-01-01 Epub Date: 2013-01-02 DOI:10.1155/2013/687069
Aibek E Mirrakhimov, Alaa M Ali
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引用次数: 17

摘要

阻塞性睡眠呼吸暂停和血脂异常是常见的医学疾病,可独立增加血管发病率和死亡率。目前的动物和人类数据表明,阻塞性睡眠呼吸暂停确实可能介导胆固醇和甘油三酯代谢的病理改变。所涉及的机制是增加脂肪分解,减少脂蛋白清除和增加肝脏的脂质输出。人类证据表明,持续气道正压治疗阻塞性睡眠呼吸暂停可改善餐后高脂血症。然而,需要更多的研究来阐明阻塞性睡眠呼吸暂停和血脂异常之间相互关系的病理生理学,以及治疗阻塞性睡眠呼吸暂停是否会导致血脂水平的改善,更重要的是,减少高脂血症相关的血管结局。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Pathobiology of obstructive sleep apnea-related dyslipidemia: focus on the liver.

Pathobiology of obstructive sleep apnea-related dyslipidemia: focus on the liver.

Obstructive sleep apnea and dyslipidemia are common medical disorders that independently increase vascular morbidity and mortality. Current animal and human data show that, indeed, obstructive sleep apnea may mediate pathological alterations in cholesterol and triglyceride metabolism. The mechanisms involved are increased lipolysis, decreased lipoprotein clearance, and enhanced lipid output from the liver. Human evidence shows that the treatment of obstructive sleep apnea with continuous positive airway pressure leads to an improvement of postprandial hyperlipidemia. However, more studies are needed, to clarify the pathophysiology of the interrelationship between obstructive sleep apnea and dyslipidemia and whether treatment of obstructive sleep apnea will lead to an improvement in the lipid profile and, more importantly, reduce hyperlipidemia-related vascular outcomes.

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