Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21224, USA.
Drugs. 2009;69 Suppl 2:13-27. doi: 10.2165/11531150-000000000-00000.
Over the past decade substantial evidence has accumulated implicating disorders of sleep in the pathogenesis of various metabolic abnormalities. This review, which is based on workshop discussions that took place at the 6th annual meeting of the International Sleep Disorders Forum: The Art of Good Sleep 2008 and a systematic literature search, provides a critical analysis of the available evidence implicating sleep disorders such as obstructive sleep apnoea (OSA), insomnia, short or long-term sleep duration and restless legs syndrome as potential risk factors for insulin resistance, glucose intolerance, type 2 diabetes mellitus and the metabolic syndrome. The review also highlights the evidence on whether treatment of specific sleep disorders can decrease metabolic risk. In total, 83 published reports were selected for inclusion. Although several studies show clear associations between sleep disorders and altered glucose metabolism, causal effects and the underlying pathophysiological mechanisms involved have not been fully elucidated. OSA appears to have the strongest association with insulin resistance, glucose intolerance, type 2 diabetes and the metabolic syndrome. There are, however, limited data supporting the hypothesis that effective treatment of sleep disorders, including OSA, has a favourable effect on glucose metabolism. Large randomized trials are thus required to address whether improvement of sleep quality and quantity can curtail excess metabolic risk. Research is also required to elucidate the mechanisms involved and to determine whether the effects of treatment for sleep disorders on glucose metabolism are dependent on the specific patient factors, the type of disorder and the duration of metabolic dysfunction. In conclusion, there is limited evidence on whether sleep disorders alter glucose metabolism and whether treatment can reduce the excess metabolic risk.
在过去的十年中，大量证据表明睡眠障碍与各种代谢异常的发病机制有关。本综述基于 2008 年第六届国际睡眠障碍论坛年度会议的专题讨论和系统文献检索，对睡眠障碍（如阻塞性睡眠呼吸暂停、失眠、睡眠时间长短和不宁腿综合征）作为胰岛素抵抗、葡萄糖耐量异常、2 型糖尿病和代谢综合征潜在危险因素的相关证据进行了批判性分析。该综述还强调了治疗特定睡眠障碍是否可以降低代谢风险的证据。总共选择了 83 篇已发表的报告。尽管有几项研究表明睡眠障碍与葡萄糖代谢改变之间存在明确的关联，但因果关系和涉及的潜在病理生理机制尚未完全阐明。阻塞性睡眠呼吸暂停似乎与胰岛素抵抗、葡萄糖耐量异常、2 型糖尿病和代谢综合征的相关性最强。然而，支持治疗睡眠障碍（包括阻塞性睡眠呼吸暂停）对葡萄糖代谢有积极影响的假设的数据有限。因此，需要进行大规模的随机试验来确定改善睡眠质量和数量是否可以减少过多的代谢风险。还需要研究阐明相关机制，并确定治疗睡眠障碍对葡萄糖代谢的影响是否取决于特定的患者因素、疾病类型和代谢功能障碍的持续时间。总之，关于睡眠障碍是否改变葡萄糖代谢以及治疗是否可以降低过多的代谢风险，证据有限。
