Blood-Brain Barrier Group, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA, 70808, USA.
J Mol Neurosci. 2013 Nov;51(3):1038-45. doi: 10.1007/s12031-013-0093-6. Epub 2013 Aug 18.
Excessive obesity correlates with hypersomnolence and impaired cognitive function, presumably induced by metabolic factors and cytokines. Production of the adipokine leptin correlates with the amount of adiposity, and leptin has been shown to promote sleep. To determine whether leptin plays a major role in the hypersomnolence of obesity, we measured sleep architecture in pan-leptin receptor knockout (POKO) mice that do not respond to leptin because of the production of a mutant, non-signaling receptor. The obese POKO mice had more non-rapid eye movement (NREM) sleep and less waking time than their littermate controls. This was mainly seen during the light span, although increased bouts of rapid eye movement sleep were also seen in the dark span. The increase of NREM sleep correlated with the extent of obesity. The POKO mice also had decreased locomotor activity and more immobility in the open field test, but there was no increase of forced immobility nor reduction of sucrose intake as would be seen in depression. The increased NREM sleep and reduced locomotor activity in the POKO mice suggest that it was obesity, rather than leptin signaling, that played a predominant role in altering sleep architecture and activity.
肥胖与嗜睡和认知功能障碍相关，这可能是由代谢因素和细胞因子引起的。脂联素的产生与脂肪量有关，并且已经证明脂联素可以促进睡眠。为了确定瘦素是否在肥胖的嗜睡中起主要作用，我们测量了不能对瘦素做出反应的全瘦素受体敲除（POKO）小鼠的睡眠结构，因为它们产生了一种突变的、无信号的受体。肥胖的 POKO 小鼠比它们的同窝对照小鼠有更多的非快速眼动（NREM）睡眠和更少的清醒时间。这主要发生在光照时段，尽管在黑暗时段也观察到快速眼动睡眠的发作增加。NREM 睡眠的增加与肥胖的程度相关。POKO 小鼠在旷场测试中也表现出运动活动减少和更多的不动，但是没有强迫不动的增加，也没有蔗糖摄入的减少，这在抑郁症中会出现。POKO 小鼠的 NREM 睡眠增加和运动活动减少表明，是肥胖而不是瘦素信号在改变睡眠结构和活动方面起主要作用。
