수면 무호흡과 대사성 기능 부전(대사성 증후군)

Abstract

The metabolic syndrome represents a clustering of several interrelated risk factors of metabolic origin that are thought to increase cardiovascular risk. One metabolic abnormality that may underlie several clinical characteristics of the metabolic syndrome is insulin resistance. The evidence that obstructive sleep apnea may independently lead to the development of both insulin resistance and individual clinical components of the metabolic syndrome, has been accumulated. Continuous positive airway pressure treatment for sleep apnea may be helpful for improvement of metabolic syndrome although the evidence is still insufficient. Intermittent hypoxemia and sleep fragmentation in sleep apnea can trigger a cascade of pathophysiological events, including autonomic activation, alterations in neuroendocrine function, and release of potent proinflammatory mediators such as tumor necrosis factor-α and interleukin-6. The converse may also be true, in that metabolic abnormalities associated with the metabolic syndrome and insulin resistance may potentially exacerbate sleep apnea and daytime sleepiness. The notion that sleep apnea exert detrimental metabolic effects may help explain the increasing prevalence of the metabolic syndrome and insulin resistance in the general population, and may have important therapeutic implications to combat the metabolic and cardiovascular disease.