Sleep deprivation and energy balance

描述（由申请人提供）：最近的流行病学研究表明，睡眠时间短（d5-7 h/night）与超重和肥胖相关，因此睡眠时间短的个体往往比睡眠8-9 h/night的个体具有更高的体重指数（BMI）。这种关系的机制目前尚不清楚。然而，能量平衡必须被破坏才能产生体重增加。因此，本研究的目的是检查短睡眠时间（4小时/晚）相对于习惯性睡眠时间（8-9小时/晚）对能量平衡的影响。本研究的主要目的是比较习惯性睡眠和短睡眠期间的能量消耗和能量摄入，并检查习惯性睡眠和短睡眠期间饮食行为所涉及的神经和激素通路。将招募30-45岁和BMI {22-25} kg/m2的男性和女性参与这项短期和习惯性睡眠期的随机交叉研究。在每{5}个晚上期间，受试者将被要求在实验室中在监督下睡觉。在此期间，受试者将全部住院，以确保依从方案。每个睡眠持续时间将由2-4周的洗脱期分隔。在每个阶段的第一天，将给予受试者一剂双标记水，以测量6天期间的自由生活能量消耗。在最初的4天里，将控制能量摄入，并在固定时间提供膳食。最后2天将自由进食自选食物。}将在禁食状态下每天评估激素，包括瘦素、胰岛素、生长激素释放肽、{PYY、脂联素和GLP-1}{并且在第4天，在24小时的时间段内，同时受试者消耗具有固定进餐时间的受控饮食}。在第5天，将进行对食物刺激的大脑活动的功能性磁共振成像测量，以检查与进食动机相关的大脑区域。在第5天，受试者将接受{使用间接热量测定法的基础代谢率}的测量。将在第5天和第6天评估自由采食量。将每晚进行多导睡眠图监测{以评估睡眠持续时间}。中介分析将使我们能够确定激素水平是否与能量消耗和能量摄入数据相关并可预测。这项研究中进行的测量将使我们能够确定睡眠时间减少如何影响能量平衡，并可能导致体重变化。因此，它将提供与能量平衡相关的神经，生理，激素和行为网络的综合信息，并受睡眠时间的影响。 公共卫生相关性：观察和流行病学研究发现，肥胖和睡眠时间短之间存在联系，在过去几十年中，两者的流行率都在增加。目前，尚不清楚睡眠不足是否是肥胖的原因，以及睡眠不足如何导致肥胖。一些研究将睡眠不足与刺激食欲的激素水平升高联系起来。这项研究将研究食物摄入和能量消耗如何通过睡眠时间来改变，以了解潜在的因果途径。

DESCRIPTION (provided by applicant): Recent epidemiological studies show that short sleep duration (d5-7 h/night) correlates with overweight and obesity, such that individuals with short sleep periods tend to have a higher body mass index (BMI) than those who sleep 8-9 h/night. The mechanism for this relationship is currently unknown. However, energy balance must be disrupted to produce weight gain. Therefore, the purpose of this study is to examine the impact of short sleep duration, 4 h/night, relative to habitual sleep duration of 8-9 h/night, on energy balance. The major aims of this study are to compare energy expenditure and energy intake during the periods of habitual and short sleep duration and to examine the neural and hormonal pathways involved in eating behavior under periods of habitual and short sleep. Men and women, 30-45 y and BMI {22-25} kg/m2, will be recruited to participate in this randomized, crossover study of short and habitual sleep periods. During each period of {5} nights, subjects will be required to sleep at the laboratory under supervision. During this time, subjects will be total inpatients to ensure compliance with the protocol. Each sleep duration period will be separated by a 2-4-wk washout period. On the first day of each phase, subjects will be given a dose of doubly-labeled water to measure free-living energy expenditure over the 6-d period. {During the first 4 days, energy intake will be controlled and meals served at fixed times. The last 2 days will be ad libitum feeding of self-selected meals.} Hormones, including leptin, insulin, ghrelin, {PYY, adiponectin, and GLP-1} will be assessed daily in the fasted state {and, on day 4, over a 24- hour period, while subjects are consuming a controlled diet with fixed meal times}. Functional magnetic resonance imaging measurements of brain activity in response to food stimuli will be done on day 5 to examine brain regions associated with motivation to eat. On day 5, subjects will undergo measurements of {basal metabolic rate using indirect calorimetry}. Ad libitum energy intakes will be assessed on days 5 and 6. Polysomnographic monitoring will be performed nightly {to assess sleep duration}. Mediation analyses will allow us to determine whether hormone levels are related to and predictive of energy expenditure and energy intake data. The measurements performed in this study will allow us to determine how reduced sleep periods can impact energy balance and potentially lead to changes in body weight. As such, it will provide comprehensive information of the neural, physiological, hormonal, and behavioral networks related to energy balance and which are affected by sleep duration. PUBLIC HEALTH RELEVANCE: Observational and epidemiological studies have found a link between obesity and short sleep duration with the prevalence of both increasing in the past decades. At this time, it is unknown whether short sleep is a cause of obesity and how short sleep would lead to obesity. Some studies associate short sleep with increased levels of hormone that stimulate appetite. This study will examine how food intake and energy expenditure can be modified by sleep duration as a means of understanding a potential causal pathway.