Department of Neurology, The Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
PLoS One. 2011;6(8):e22987. doi: 10.1371/journal.pone.0022987. Epub 2011 Aug 11.
Chronic sleep disruption in laboratory rats leads to increased energy expenditure, connective tissue abnormalities, and increased weights of major organs relative to body weight. Here we report on expanded findings and the extent to which abnormalities become long-lasting, potentially permanent changes to health status after apparent recuperation from chronic sleep disruption. Rats were exposed 6 times to long periods of disrupted sleep or control conditions during 10 weeks to produce adaptations and then were permitted nearly 4 months of undisturbed sleep. Measurements were made in tissues from these groups and in preserved tissue from the experimental and control groups of an antecedent study that lacked a lengthy recuperation period. Cycles of sleep restriction resulted in energy deficiency marked by a progressive course of hyperphagia and major (15%) weight loss. Analyses of tissue composition in chronically sleep-restricted rats indicated that protein and lipid amounts in internal organs were largely spared, while adipose tissue depots appeared depleted. This suggests high metabolic demands may have preserved the size of the vital organs relative to expectations of severe energy deficiency alone. Low plasma corticosterone and leptin concentrations appear to reflect low substrate availability and diminished adiposity. After nearly 4 months of recuperation, sleep-restricted rats were consuming 20% more food and 35% more water than did comparison control rats, despite normalized weight, normalized adipocytes, and elevated plasma leptin concentrations. Plasma cholesterol levels in recuperated sleep-restricted rats were diminished relative to those of controls. The chronically increased intake of nutriments and water, along with altered negative feedback regulation and substrate use, indicate that internal processes are modified long after a severe period of prolonged and insufficient sleep has ended.
慢性睡眠剥夺会导致实验大鼠的能量消耗增加、结缔组织异常以及主要器官的重量相对于体重增加。在这里，我们报告了更广泛的发现，以及在慢性睡眠剥夺后明显恢复期间，这些异常是否会持续存在，甚至可能成为健康状况的永久性变化。在 10 周的时间里，大鼠经历了 6 次长时间的睡眠中断或对照条件，以产生适应性，然后允许它们有近 4 个月的不受干扰的睡眠。对这些组的组织进行了测量，并对缺乏长时间恢复期的先前研究的实验组和对照组的保存组织进行了测量。睡眠限制周期导致能量不足，表现为暴食和体重显著（15%）下降的进行性过程。对慢性睡眠受限大鼠的组织成分分析表明，内部器官的蛋白质和脂质含量基本不受影响，而脂肪组织储存似乎被耗尽。这表明，高代谢需求可能使重要器官的大小相对于仅严重能量不足的预期得以维持。低血浆皮质酮和瘦素浓度似乎反映了底物可用性降低和脂肪减少。在近 4 个月的恢复期后，睡眠受限大鼠比对照组大鼠多消耗 20%的食物和 35%的水，尽管体重、脂肪细胞和血浆瘦素浓度都正常。恢复期睡眠受限大鼠的血浆胆固醇水平相对低于对照组。长期摄入营养物质和水，以及改变的负反馈调节和底物利用，表明在严重的长期睡眠不足结束后，内部过程会发生长期改变。
