Abstract
Metabolic syndrome (MS) is a diverse condition linked to an elevated risk of
cardiovascular issues. Emerging evidence from various types of research, including
experimental, translational, and clinical studies, has indicated that obstructive sleep
apnoea (OSA) is connected to both existing and newly developing aspects of MS. The
plausible biological explanation centers primarily around one of OSA's main features,
intermittent hypoxia. This leads to heightened sympathetic activity with cardiovascular
consequences, increased liver glucose production, insulin resistance due to
inflammation in adipose tissue, dysfunction in pancreatic β-cells, elevated lipid levels
through deteriorating fasting lipid profiles, and decreased removal of triglyceride-rich
lipoproteins.
While several interconnected pathways exist, the clinical evidence primarily relies on
observational data, making it difficult to establish causality. The co-occurrence of
visceral obesity and potential confounding factors like medications complicates the
assessment of OSA's independent impact on MS. In this chapter, we re-evaluate the
evidence regarding how OSA and intermittent hypoxia may contribute to adverse
effects on MS parameters independently of body fat. We place particular emphasis on
recent findings from intervention studies. This chapter outlines the research gaps, the
challenges faced in the field, potential directions for future exploration, and the
necessity for more high-quality data from intervention studies that address the
influence of both established and promising therapies for OSA and obesity.
Keywords: Cardiovascular issues, Metabolic syndrome, Obesity, Obstructive sleep apnoea, Sleep apnoea.