Department of Integrative Physiology, Sleep and Chronobiology Laboratory, University of Colorado, Boulder, CO, USA.
Nat Sci Sleep. 2009 Dec 16;2:9-18. doi: 10.2147/nss.s7624. Print 2010.
The neurobiology of circadian, wakefulness-sleep, and feeding systems interact to influence energy homeostasis. Sleep and circadian disruptions are reported to be associated with increased risk of diabetes and obesity, yet the roles of energy balance hormones in these associations are largely unknown. Therefore, in the current study we aimed to assess the influence of several weeks of circadian misalignment (sleep and wakefulness occurring at an inappropriate biological time) on the anorexigenic adipocyte hormone leptin. We utilized data from a previous study designed to assess physiological and cognitive consequences of changes in day length and light exposure as may occur during space fight, including exploration class space missions and exposure to the Martian Sol (day length). We hypothesized that circadian misalignment during an exploration class spaceflight simulation would reduce leptin levels. Following a three-week ~8 hours per night home sleep schedule, 14 healthy participants lived in the laboratory for more than one month. After baseline data collection, participants were scheduled to either 24.0 or 24.6 hours of wakefulness-sleep schedules for 25 days. Changes in the phase of the circadian melatonin rhythm, sleep, and leptin levels were assessed. Half of participants analyzed exhibited circadian misalignment with an average change in phase angle from baseline of ~4 hours and these participants showed reduced leptin levels, sleep latency, stage 2 and total sleep time (7.3 to 6.6 hours) and increased wakefulness after sleep onset (all P < 0.05). The control group remained synchronized and showed significant increases in sleep latency and leptin levels. Our findings indicate that weeks of circadian misalignment, such as that which occurs in circadian sleep disorders, alters leptin levels and therefore may have implications for appetite and energy balance.
昼夜节律、睡眠觉醒和摄食系统的神经生物学相互作用影响能量稳态。睡眠和昼夜节律紊乱与糖尿病和肥胖风险增加有关，但能量平衡激素在这些关联中的作用在很大程度上尚不清楚。因此，在目前的研究中，我们旨在评估数周的昼夜节律失调（睡眠时间和觉醒时间不适当的生物时间）对厌食性脂肪激素瘦素的影响。我们利用了先前研究的数据，该研究旨在评估可能发生在太空飞行期间的日长和光照暴露变化的生理和认知后果，包括探索级太空任务和暴露于火星 Sol（日长）。我们假设在探索级太空飞行模拟期间的昼夜节律失调会降低瘦素水平。在遵循每晚 8 小时的家庭睡眠时间表三周后，14 名健康参与者在实验室中生活了一个多月。在基线数据收集后，参与者被安排进行 25 天的 24.0 或 24.6 小时的睡眠-觉醒时间表。评估了昼夜节律褪黑素节律、睡眠和瘦素水平的变化。分析的一半参与者表现出昼夜节律失调，平均相位角从基线变化约 4 小时，这些参与者表现出瘦素水平降低、睡眠潜伏期、第 2 阶段和总睡眠时间（7.3 至 6.6 小时）和睡眠后觉醒时间增加（所有 P < 0.05）。对照组保持同步，睡眠潜伏期和瘦素水平显著增加。我们的研究结果表明，数周的昼夜节律失调，如在昼夜节律睡眠障碍中发生的那样，会改变瘦素水平，因此可能对食欲和能量平衡产生影响。
