Minnesota Obesity Prevention Training Program, School of Public Health, University of Minnesota, Minneapolis, MN, USA.
Neurosci Biobehav Rev. 2012 Mar;36(3):1015-29. doi: 10.1016/j.neubiorev.2012.01.001. Epub 2012 Jan 16.
The rapid rise in obesity prevalence in the modern world parallels a significant reduction in restorative sleep (Agras et al., 2004; Dixon et al., 2007, 2001; Gangwisch and Heymsfield, 2004; Gupta et al., 2002; Sekine et al., 2002; Vioque et al., 2000; Wolk et al., 2003). Reduced sleep time and quality increases the risk for obesity, but the underlying mechanisms remain unclear (Gangwisch et al., 2005; Hicks et al., 1986; Imaki et al., 2002; Jennings et al., 2007; Moreno et al., 2006). A majority of the theories linking human sleep disturbances and obesity rely on self-reported sleep. However, studies with objective measurements of sleep/wake parameters suggest a U-shaped relationship between sleep and obesity. Studies in animal models are needed to improve our understanding of the association between sleep disturbances and obesity. Genetic and experimenter-induced models mimicking characteristics of human obesity are now available and these animal models will be useful in understanding whether sleep disturbances determine propensity for obesity, or result from obesity. These models exhibit weight gain profiles consistently different from control animals. Thus a careful evaluation of animal models will provide insight into the relationship between sleep disturbances and obesity in humans. In this review we first briefly consider the fundamentals of sleep and key sleep disturbances, such as sleep fragmentation and excessive daytime sleepiness (EDS), observed in obese individuals. Then we consider sleep deprivation studies and the role of circadian alterations in obesity. We describe sleep/wake changes in various rodent models of obesity and obesity resistance. Finally, we discuss possible mechanisms linking sleep disturbances with obesity.
在现代世界，肥胖症的患病率迅速上升，与此同时，恢复性睡眠（Agras 等人，2004 年；Dixon 等人，2007 年，2001 年；Gangwisch 和 Heymsfield，2004 年；Gupta 等人，2002 年；Sekine 等人，2002 年；Vioque 等人，2000 年；Wolk 等人，2003 年）显著减少。睡眠时间和质量的减少会增加肥胖的风险，但潜在机制仍不清楚（Gangwisch 等人，2005 年；Hicks 等人，1986 年；Imaki 等人，2002 年；Jennings 等人，2007 年；Moreno 等人，2006 年）。将人类睡眠障碍与肥胖联系起来的大多数理论都依赖于自我报告的睡眠。然而，对睡眠/觉醒参数进行客观测量的研究表明，睡眠与肥胖之间存在 U 型关系。需要在动物模型中进行研究，以增进我们对睡眠障碍与肥胖之间关联的理解。目前已经有模拟人类肥胖特征的遗传和实验诱导模型，这些动物模型将有助于了解睡眠障碍是否决定肥胖倾向，或者是否由肥胖引起。这些模型表现出与对照动物明显不同的体重增加模式。因此，对动物模型进行仔细评估将有助于深入了解人类睡眠障碍与肥胖之间的关系。在这篇综述中，我们首先简要考虑睡眠的基本原理和肥胖个体中观察到的关键睡眠障碍，如睡眠碎片化和白天过度嗜睡（EDS）。然后，我们考虑睡眠剥夺研究和昼夜节律改变在肥胖中的作用。我们描述了各种肥胖和肥胖抵抗啮齿动物模型的睡眠/觉醒变化。最后，我们讨论了将睡眠障碍与肥胖联系起来的可能机制。
