Department of Pathophysiology, University of Split School of Medicine, 21000 Split, Croatia.
Department of Cardiology, University Hospital of Split, 21000 Split, Croatia.
Int J Mol Sci. 2024 Mar 13;25(6):3243. doi: 10.3390/ijms25063243.
Obstructive sleep apnoea (OSA) and components of metabolic syndrome (MetS) are inextricably connected. Considering the increasing burden of MetS and OSA, in the present review, we aimed to collate and summarise the potential pathophysiological mechanisms linking these pathologies. In short, obesity appears to promote OSA development via multiple pathways, some of which are not directly related to mass but rather to metabolic complications of obesity. Simultaneously, OSA promotes weight gain through central mechanisms. On the other hand, diabetes mellitus contributes to OSA pathophysiology mainly through effects on peripheral nerves and carotid body desensitization, while intermittent hypoxia and sleep fragmentation are the principal culprits in OSA-mediated diabetes. Apart from a bidirectional pathophysiological relationship, obesity and diabetes mellitus together additively increase cardiovascular risk in OSA patients. Additionally, the emergence of new drugs targeting obesity and unequivocal results of the available studies underscore the need for further exploration of the mechanisms linking MetS and OSA, all with the aim of improving outcomes in these patients.
阻塞性睡眠呼吸暂停(OSA)和代谢综合征(MetS)的各个组分紧密相关。鉴于 MetS 和 OSA 的负担不断增加,在本综述中,我们旨在整理和总结这些疾病之间潜在的病理生理学机制。简而言之,肥胖似乎通过多种途径促进 OSA 的发展,其中一些途径与体重无关,而是与肥胖的代谢并发症有关。同时,OSA 通过中枢机制促进体重增加。另一方面,糖尿病主要通过对周围神经和颈动脉体脱敏的影响来影响 OSA 的病理生理学,而间歇性缺氧和睡眠片段化是 OSA 导致糖尿病的主要原因。除了双向病理生理学关系外,肥胖和糖尿病共同增加 OSA 患者的心血管风险。此外,针对肥胖的新药的出现和现有研究的明确结果强调了需要进一步探索 MetS 和 OSA 之间的联系机制,所有这些都是为了改善这些患者的预后。