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阻塞性睡眠呼吸暂停与血脂异常:对动脉粥样硬化的影响。

Obstructive sleep apnea and dyslipidemia: implications for atherosclerosis.

机构信息

Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

出版信息

Curr Opin Endocrinol Diabetes Obes. 2010 Apr;17(2):161-5. doi: 10.1097/MED.0b013e3283373624.

DOI:10.1097/MED.0b013e3283373624
PMID:20125003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2904751/
Abstract

PURPOSE OF REVIEW

The aim of this review is to summarize current evidence about the impact of obstructive sleep apnea (OSA) and intermittent hypoxia on dyslipidemia and provide future perspectives in this area.

RECENT FINDINGS

Intermittent hypoxia, a hallmark of OSA, induces hyperlipidemia in lean mice. Hyperlipidemia of intermittent hypoxia occurs, at least in part, due to activation of the transcription factor sterol regulatory element-binding protein-1 (SREBP-1) and an important downstream enzyme of triglyceride and phospholipid biosynthesis, stearoyl-CoA desaturase-1. Furthermore, intermittent hypoxia may regulate SREBP-1 and stearoyl-CoA desaturase-1 via the transcription factor hypoxia-inducible factor 1. In contrast, key genes involved in cholesterol biosynthesis, SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, are unaffected by intermittent hypoxia. In humans, there is no definitive evidence regarding the effect of OSA on dyslipidemia. Several cross-sectional studies suggest that OSA is independently associated with increased levels of total cholesterol, low-density lipoprotein and triglycerides, whereas others report no such relationship. Some nonrandomized and randomized studies show that OSA treatment with continuous positive airway pressure may have a beneficial effect on lipid profile.

SUMMARY

There is increasing evidence that intermittent hypoxia is independently associated with dyslipidemia. However, the role of OSA in causality of dyslipidemia remains to be established.

摘要

目的综述

本文旨在总结阻塞性睡眠呼吸暂停(OSA)和间歇性低氧对血脂异常影响的最新证据,并对该领域的未来发展提供展望。

最近的发现

间歇性低氧是 OSA 的一个标志,它会导致瘦鼠发生高脂血症。间歇性低氧引起的高脂血症至少部分归因于转录因子固醇调节元件结合蛋白-1(SREBP-1)的激活,以及甘油三酯和磷脂生物合成的重要下游酶硬脂酰辅酶 A 去饱和酶-1。此外,间歇性低氧可能通过转录因子缺氧诱导因子 1来调节 SREBP-1 和硬脂酰辅酶 A 去饱和酶-1。相比之下,胆固醇生物合成的关键基因 SREBP-2 和 3-羟-3-甲基戊二酰辅酶 A(HMG-CoA)还原酶不受间歇性低氧的影响。在人类中,关于 OSA 对血脂异常的影响尚无明确证据。一些横断面研究表明,OSA 与总胆固醇、低密度脂蛋白和甘油三酯水平升高独立相关,而其他研究则没有发现这种关系。一些非随机和随机研究表明,持续气道正压通气治疗 OSA 可能对血脂谱有有益的影响。

总结

越来越多的证据表明,间歇性低氧与血脂异常独立相关。然而,OSA 在血脂异常因果关系中的作用仍有待确定。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d771/2904751/f2991c9eed65/nihms213357f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d771/2904751/f2991c9eed65/nihms213357f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d771/2904751/f2991c9eed65/nihms213357f1.jpg

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