Obstructive sleep apnea and metabolic syndrome

Abstract Metabolic syndrome (MS) is a heterogeneous condition associated with increased cardiovascular risk. There is growing evidence from experimental, translational, and clinical investigations that has suggested that obstructive sleep apnea (OSA) is associated with prevalent and incident components of MS and MS itself. The biological plausibility is supportive, primarily related to one of the main features of OSA, namely intermittent hypoxia: increased sympathetic activation with hemodynamic repercussions, increased hepatic glucose output, insulin resistance through adipose tissue inflammation, pancreatic β‐cell dysfunction, hyperlipidemia through the worsening of fasting lipid profiles, and the reduced clearance of triglyceride‐rich lipoproteins. Although there are multiple related pathways, the clinical evidence relies mainly on cross‐sectional data preventing any causality assumptions. The overlapping presence of visceral obesity or other confounders such as medications challenges the ability to understand the independent contribution of OSA on MS. In this review, we revisit the evidence on how OSA/intermittent hypoxia could mediate adverse effects of MS parameters independent of adiposity. Particular attention is devoted to discussing recent evidence from interventional studies. This review describes the research gaps, the challenges in the field, perspectives, and the need for additional high‐quality data from interventional studies addressing the impact of not only established but promising therapies for OSA/obesity.