Dept. of Psychobiology, Universidade Federal de São Paulo, Brazil.
Am J Physiol Endocrinol Metab. 2010 Mar;298(3):E726-34. doi: 10.1152/ajpendo.00660.2009. Epub 2010 Jan 5.
Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25-35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.
有几项证据表明，睡眠时间在体重控制中起着作用。然而，人们一直认为，在发现食欲素（下丘脑分泌素）之后，睡眠与能量稳态之间相互作用的分子基础已经得到了阐明。然而，没有研究验证过在睡眠剥夺引起的暴食期间，神经肽 Y（NPY）和食欲素变化之间的关系。在本研究中，我们旨在确定 Wistar 大鼠在平台法睡眠剥夺（从 24 小时到 96 小时）或睡眠限制 21 天（SR-21d）后，代谢物、内分泌和下丘脑神经肽表达的变化时间进程。尽管应激激素发生了变化，但我们在 SR-21d 组中没有发现食物摄入量和体重的变化。然而，睡眠剥夺大鼠的食物摄入量从第 72 小时开始增加了 25-35%，同时体重略有下降。这种变化与下丘脑前食欲素（PPO）mRNA 水平在 24 小时时的增加有关，接着在睡眠剥夺 48 小时时 NPY 增加。相反，睡眠恢复降低了 PPO 和 NPY 的表达，这迅速使动物处于厌食状态。我们的数据还支持，睡眠剥夺会迅速增加能量消耗，从而导致负能平衡和肝脏糖原及血清三酰甘油水平降低，尽管出现了暴食。有趣的是，这些变化与血清中胰高血糖素、皮质酮和去甲肾上腺素水平的升高有关，但对瘦素、胰岛素或胃饥饿素没有影响。总之，食欲素的激活解释了睡眠剥夺引起的众多变化，尤其是在应激和负能平衡下引起的暴食。
