Koban Michael, Sita Luciane V, Le Wei Wei, Hoffman Gloria E
Laboratory of Physiology, Richard N. Dixon Science Research Center, Department of Biology, Morgan State University, Baltimore, MD, USA.
Sleep. 2008 Jul;31(7):927-33.
Chronic sleep deprivation of rats causes hyperphagia without body weight gain. Sleep deprivation hyperphagia is prompted by changes in pathways governing food intake; hyperphagia may be adaptive to sleep deprivation hypermetabolism. A recent paper suggested that sleep deprivation might inhibit ability of rats to increase food intake and that hyperphagia may be an artifact of uncorrected chow spillage. To resolve this, a palatable liquid diet (Ensure) was used where spillage is insignificant.
Sleep deprivation of male Sprague Dawley rats was enforced for 10 days by the flowerpot/platform paradigm. Daily food intake and body weight were measured. On day 10, rats were transcardially perfused for analysis of hypothalamic mRNA expression of the orexigen, neuropeptide Y (NPY).
Morgan State University, sleep deprivation and transcardial perfusion; University of Maryland, NPY in situ hybridization and analysis.
Using a liquid diet for accurate daily measurements, there was no change in food intake in the first 5 days of sleep deprivation. Importantly, from days 6-10 it increased significantly, peaking at 29% above baseline. Control rats steadily gained weight but sleep-deprived rats did not. Hypothalamic NPY mRNA levels were positively correlated to stimulation of food intake and negatively correlated with changes in body weight.
Sleep deprivation hyperphagia may not be apparent over the short term (i.e., < or = 5 days), but when extended beyond 6 days, it is readily observed. The timing of changes in body weight and food intake suggests that the negative energy balance induced by sleep deprivation prompts the neural changes that evoke hyperphagia.
大鼠长期睡眠剥夺会导致食欲亢进但体重并未增加。睡眠剥夺引起的食欲亢进是由控制食物摄入的途径变化所引发的;食欲亢进可能是对睡眠剥夺所致高代谢的一种适应性反应。最近有一篇论文指出,睡眠剥夺可能会抑制大鼠增加食物摄入的能力,且食欲亢进可能是未纠正的食物溢出造成的假象。为解决这一问题,采用了一种可口的流食(安素),其溢出量可忽略不计。
采用花盆/平台范式对雄性斯普拉格-道利大鼠进行为期10天的睡眠剥夺。测量每日食物摄入量和体重。在第10天,对大鼠进行心脏灌注,以分析下丘脑促食欲肽神经肽Y(NPY)的mRNA表达。
摩根州立大学,睡眠剥夺及心脏灌注实验;马里兰大学,NPY原位杂交及分析。
使用流食进行精确的每日测量,睡眠剥夺的前5天食物摄入量没有变化。重要的是,从第6天到第10天,食物摄入量显著增加,峰值比基线高出29%。对照大鼠体重稳步增加,但睡眠剥夺的大鼠体重未增加。下丘脑NPY mRNA水平与食物摄入刺激呈正相关,与体重变化呈负相关。
睡眠剥夺引起的食欲亢进在短期内(即≤5天)可能不明显,但超过6天则很容易观察到。体重和食物摄入变化的时间表明,睡眠剥夺引起的负能量平衡促使了引发食欲亢进的神经变化。