Servicio de Neumología, Hospital Montecelo, Pontevedra, Spain.
Servicio de Neumología, Hospital Universitario La Paz-IdiPAZ, Madrid, Spain.
Sleep. 2019 Mar 1;42(3). doi: 10.1093/sleep/zsy236.
Lipid metabolism deregulation constitutes the pathogenic basis for the development of atherosclerosis and justifies a high incidence of cardiovascular-related morbidity and mortality. Some data suggest that dyslipidemia may be associated with sleep-disordered breathing, mainly obstructive sleep apnea (OSA), due to alterations in fundamental biochemical processes, such as intermittent hypoxia (IH). The aim of this systematic review was to identify and critically evaluate the current evidence supporting the existence of a possible relationship between OSA and alterations in lipid metabolism. Much evidence shows that, during the fasting state, OSA and IH increase lipid delivery from the adipose tissue to the liver through an up-regulation of the sterol regulatory element-binding protein-1 and stearoyl-CoA desaturase-1, increasing the synthesis of cholesterol esters and triglycerides. In the postprandial state, lipoprotein clearance is delayed due to lower lipoprotein lipase activity, probably secondary to IH-up-regulation of angiopoietin-like protein 4 and decreased activity of the peroxisome proliferator-activated receptor alpha. Moreover, oxidative stress can generate dysfunctional oxidized lipids and reduce the capacity of high-density lipoproteins (HDL) to prevent low-density lipoprotein (LDL) oxidation. In the clinical field, several observational studies and a meta-regression analysis support the existence of a link between OSA and dyslipidemia. Although there is evidence of improved lipid profile after apnea-hypopnea suppression with continuous positive airway pressure (CPAP), the majority of the data come from observational studies. In contrast, randomized controlled trials evaluating the effects of CPAP on lipid metabolism present inconclusive results and two meta-analyses provide contradictory evidence.
脂质代谢紊乱是动脉粥样硬化发展的致病基础，也是心血管相关发病率和死亡率高的原因。一些数据表明，由于基本生化过程的改变，如间歇性低氧（IH），血脂异常可能与睡眠呼吸障碍有关，主要是阻塞性睡眠呼吸暂停（OSA）。本系统评价的目的是确定和批判性评估当前支持 OSA 与脂质代谢改变之间可能存在关系的证据。大量证据表明，在禁食状态下，OSA 和 IH 通过上调固醇调节元件结合蛋白-1 和硬脂酰辅酶 A 去饱和酶-1，增加胆固醇酯和甘油三酯的合成，增加脂肪组织向肝脏的脂质输送。在餐后状态下，由于脂蛋白脂肪酶活性降低，脂蛋白清除延迟，可能继发于 IH 上调血管生成素样蛋白 4 和过氧化物酶体增殖物激活受体α活性降低。此外，氧化应激会产生功能失调的氧化脂质，并降低高密度脂蛋白（HDL）预防低密度脂蛋白（LDL）氧化的能力。在临床领域，几项观察性研究和一项荟萃回归分析支持 OSA 和血脂异常之间存在联系。尽管有证据表明，持续气道正压通气（CPAP）抑制呼吸暂停低通气后血脂谱得到改善，但大多数数据来自观察性研究。相比之下，评估 CPAP 对脂质代谢影响的随机对照试验结果不一致，两项荟萃分析提供了相互矛盾的证据。
