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相互作用的传染病?睡眠不足、胰岛素抵抗和肥胖。

Interacting epidemics? Sleep curtailment, insulin resistance, and obesity.

机构信息

Immunogenetics Section, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA.

出版信息

Ann N Y Acad Sci. 2012 Aug;1264(1):110-34. doi: 10.1111/j.1749-6632.2012.06655.x. Epub 2012 Jul 24.

Abstract

In the last 50 years, the average self-reported sleep duration in the United States has decreased by 1.5-2 hours in parallel with an increasing prevalence of obesity and diabetes. Epidemiological studies and meta-analyses report a strong relationship between short or disturbed sleep, obesity, and abnormalities in glucose metabolism. This relationship is likely to be bidirectional and causal in nature, but many aspects remain to be elucidated. Sleep and the internal circadian clock influence a host of endocrine parameters. Sleep curtailment in humans alters multiple metabolic pathways, leading to more insulin resistance, possibly decreased energy expenditure, increased appetite, and immunological changes. On the other hand, psychological, endocrine, and anatomical abnormalities in individuals with obesity and/or diabetes can interfere with sleep duration and quality, thus creating a vicious cycle. In this review, we address mechanisms linking sleep with metabolism, highlight the need for studies conducted in real-life settings, and explore therapeutic interventions to improve sleep, with a potential beneficial effect on obesity and its comorbidities.

摘要

在过去的 50 年中,美国的平均自我报告睡眠时间与肥胖症和糖尿病的患病率呈平行趋势,减少了 1.5-2 小时。流行病学研究和荟萃分析报告称,睡眠不足或睡眠紊乱、肥胖和葡萄糖代谢异常之间存在很强的关系。这种关系可能是双向的和因果关系,但仍有许多方面需要阐明。睡眠和内部生物钟会影响许多内分泌参数。人类的睡眠时间缩短会改变多种代谢途径,导致更多的胰岛素抵抗,可能减少能量消耗,增加食欲和免疫变化。另一方面,肥胖症和/或糖尿病患者的心理、内分泌和解剖异常会干扰睡眠时间和质量,从而形成恶性循环。在这篇综述中,我们探讨了将睡眠与新陈代谢联系起来的机制,强调了在实际环境中进行研究的必要性,并探讨了改善睡眠的治疗干预措施,这可能对肥胖症及其合并症有有益的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b07f/3464354/2ecd514311a0/nyas1264-0110-f1.jpg

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