Meszaros Martina, Bikov Andras
Department of Pulmonology and Sleep Disorders Centre, University Hospital Zurich, 8091 Zurich, Switzerland.
Department of Pulmonology, Semmelweis University, 1083 Budapest, Hungary.
Biomedicines. 2022 Oct 29;10(11):2754. doi: 10.3390/biomedicines10112754.
Obstructive sleep apnoea (OSA) is associated with cardiovascular and metabolic comorbidities, including hypertension, dyslipidaemia, insulin resistance and atherosclerosis. Strong evidence suggests that OSA is associated with an altered lipid profile including elevated levels of triglyceride-rich lipoproteins and decreased levels of high-density lipoprotein (HDL). Intermittent hypoxia; sleep fragmentation; and consequential surges in the sympathetic activity, enhanced oxidative stress and systemic inflammation are the postulated mechanisms leading to metabolic alterations in OSA. Although the exact mechanisms of OSA-associated dyslipidaemia have not been fully elucidated, three main points have been found to be impaired: activated lipolysis in the adipose tissue, decreased lipid clearance from the circulation and accelerated de novo lipid synthesis. This is further complicated by the oxidisation of atherogenic lipoproteins, adipose tissue dysfunction, hormonal changes, and the reduced function of HDL particles in OSA. In this comprehensive review, we summarise and critically evaluate the current evidence about the possible mechanisms involved in OSA-associated dyslipidaemia.
阻塞性睡眠呼吸暂停(OSA)与心血管和代谢合并症相关,包括高血压、血脂异常、胰岛素抵抗和动脉粥样硬化。有力证据表明,OSA与脂质谱改变有关,包括富含甘油三酯的脂蛋白水平升高和高密度脂蛋白(HDL)水平降低。间歇性缺氧、睡眠片段化以及交感神经活动的相应激增、氧化应激增强和全身炎症是导致OSA代谢改变的假定机制。尽管OSA相关血脂异常的确切机制尚未完全阐明,但已发现三个主要环节受损:脂肪组织中脂解激活、循环中脂质清除减少以及从头脂质合成加速。在OSA中,致动脉粥样硬化脂蛋白的氧化、脂肪组织功能障碍、激素变化以及HDL颗粒功能降低使情况更加复杂。在这篇综述中,我们总结并批判性地评估了有关OSA相关血脂异常可能机制的现有证据。