Obstructive sleep apnoea (OSA) is a highly prevalent disorder, which conveys an increased risk of cardiovascular disease and death. Furthermore, there is increasing evidence of an independent association of OSA with alterations in glucose metabolism leading to insulin resistance (IR), type 2 diabetes and metabolic syndrome. The underlying pathophysiology is poorly understood but intermittent hypoxia (IH) with repetitive short cycles of desaturation followed by rapid reoxygenation as hallmark feature of OSA is likely to play a key role. Inflammatory processes are central in this pathogenesis and there is ample evidence – arising from both cell culture and in vivo models – that IH preferentially activates nuclear factor-kappa B (NF-κB) – mediated pathways with the downstream consequence of expression of pro-inflammatory cytokines, chemokines and adhesion molecules that may contribute to cardiometabolic processes. OSA is closely linked to obesity and there is increasing evidence that adipose tissue is an important target organ of pro-inflammatory mediators in response to IH. Indeed, recent animal data suggest that IH induces morphological obesity-like pro-inflammatory changes in the adipose tissue which correlate with the severity of IR and may be a crucial link between OSA and the pathogenesis of disorders affecting glucose metabolism. A greater understanding of the detailed mechanisms underlying IH-induced adipose tissue inflammation should lead to the identification of therapeutic targets and therefore, further translational studies involving cell, animal and human models are strongly required.