The demands of present day living have placed a premium on time. Voluntary sleep curtailment is endemic and many adults typically sleep an average of six hours per night. Observational data suggest that short sleep duration is associated with a greater likelihood of being obese. Low grade chronic sleep deprivation may constitute an important and potentially correctable behavioral factor in the alarming increase in obesity. There are no definitive experimental studies in humans showing whether insufficient sleep indeed contributes to increased energy intake, changes in energy expenditure, and an increase in fat mass. We propose a series of novel studies to investigate abnormalities in energy homeostasis imparted by sleep restriction. These studies combine state-of-the-art techniques for monitoring sleep, food intake, energy expenditure, neuroendocrine energy regulation, body composition, and translational studies of adipocyte biology in humans. We will measure food intake, energy expenditure (basal metabolic rate, thermic effect of food, and activity), neurohormone levels, body fat content, and obtain fat biopsies for studies of adipocytes, in healthy subjects with normal BMI (20-25 kg/m2). Eighteen subjects (9 men and 9 women) will be randomized to a cross-over protocol of sleep restriction. After a 4 day baseline evaluation, these subjects will undergo 14 days of modest sleep restriction or a control period followed by a 3 day recovery period. Measurements during sleep restriction will be compared to those obtained while randomized to the control session. Sleep restriction and control sessions will undergo similar monitoring and measurements in the Clinical Research Unit over the same duration. We will test the following hypotheses: 1. that sleep restriction results in increased caloric intake 2. That sleep restriction does not change energy expenditure 3. That sleeps restriction results in a positive energy balance and increased fat mass 4. That sleep restriction results in changes in adipocyte biology that lead to impaired leptin signaling Our proposal builds on established research programs and compelling preliminary data addressing first, neuroendocrine mechanisms in sleep and obesity, and second, the regulation of energy intake and energy expenditure in humans. These studies will provide pivotal insights into whether sleep restriction promotes increased food intake and/or reduced activity levels, and increased fat mass, and into the mechanisms by which sleep interacts with energy balance and obesity risk.
We propose to examine whether 14 nights of modest sleep restriction results in increased caloric consumption without any increase in activity, resulting in an increase in body fat content. These findings will help explain whether the reduced sleep duration, endemic in the general population, may be contributing to the current epidemic of obesity, and suggest strategies to reduce this risk.
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|Medina-Inojosa, Jose; Somers, Virend; Jenkins, Sarah et al. (2017) Validation of a White-light 3D Body Volume Scanner to Assess Body Composition. Obes Open Access 3:|
|Medina-Inojosa, Jose; Somers, Virend K; Ngwa, Taiwo et al. (2016) Reliability of a 3D Body Scanner for Anthropometric Measurements of Central Obesity. Obes Open Access 2:|
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|Covassin, Naima; Somers, Virend K (2016) Somnolence: The Silent Partner in the Sleep Apnea-Hypertension Relationship. Hypertension 68:1100-1102|
|Covassin, Naima; Singh, Prachi; Somers, Virend K (2016) Keeping Up With the Clock: Circadian Disruption and Obesity Risk. Hypertension 68:1081-1090|
|Olson, Christy A; Hamilton, Nancy A; Somers, Virend K (2016) Percentage of REM sleep is associated with overnight change in leptin. J Sleep Res 25:419-25|
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|Soucek, Filip; Covassin, Naima; Singh, Prachi et al. (2015) Effects of Atorvastatin (80 mg) Therapy on Quantity of Epicardial Adipose Tissue in Patients Undergoing Pulmonary Vein Isolation for Atrial Fibrillation. Am J Cardiol 116:1443-6|
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