Diabetes and metabolic aspects of OSA

Obstructive sleep apnoea (OSA) is increasingly recognised as a risk factor for cardiometabolic dysfunction. Obesity is the most common risk factor in OSA, and various obesity-related cardiometabolic disorders, including a spectrum of glucose disorders from insulin resistance to overt type 2 diabetes mellitus, hypertension, dyslipidaemia and the metabolic syndrome, have all been found to be highly associated with sleep-disordered breathing. Current evidence on the magnitude of the impact on ultimate morbidity or mortality attributable to OSA-induced metabolic dysfunction is scarce. Given the known pathophysiology of intermittent hypoxia and sleep disturbance/loss in OSA, it is postulated that OSA independently contributes towards metabolic dysfunction through various downstream intermediary pathways of sympathetic activation, neurohumoral changes, inflammation and oxidative stress. Human and animal/cell experiments are providing clues to these mechanistic pathways. Regardless of any independent role in the causation of metabolic dysfunction, awareness of the concurrence of OSA and metabolic disorders, and the modifying roles of diet and lifestyle behaviour on metabolic function cannot be over emphasised