Context Sleep restriction alters responses to food. However, the underlying neural mechanisms for this effect are not well understood. Objective The purpose of this study was to determine whether there is a neural system that is preferentially activated in response to unhealthy compared with healthy foods. Participants Twenty-five normal-weight individuals, who normally slept 7–9 h per night, completed both phases of this randomized controlled study. Intervention Each participant was tested after a period of five nights of either 4 or 9 h in bed. Functional magnetic resonance imaging (fMRI) was performed in the fasted state, presenting healthy and unhealthy food stimuli and objects in a block design. Neuronal responses to unhealthy, relative to healthy food stimuli after each sleep period were assessed and compared. Results After a period of restricted sleep, viewing unhealthy foods led to greater activation in the superior and middle temporal gyri, middle and superior frontal gyri, left inferior parietal lobule, orbitofrontal cortex, and right insula compared with healthy foods. These same stimuli presented after a period of habitual sleep did not produce marked activity patterns specific to unhealthy foods. Further, food intake during restricted sleep increased in association with a relative decrease in brain oxygenation level-dependent (BOLD) activity observed in the right insula. Conclusion This inverse relationship between insula activity and food intake and enhanced activation in brain reward and food-sensitive centers in response to unhealthy foods provides a model of neuronal mechanisms relating short sleep duration to obesity.

Background/Objectives The extent to which alterations in energy expenditure (EE) in response to sleep restriction contribute to the short sleep-obesity relationship is not clearly defined. Short sleep may induce changes in resting metabolic rate (RMR), thermic effect of food (TEF), and postprandial substrate oxidation. Subjects/Methods Ten females (age and BMI: 22-43 y and 23.4-28 kg/m2) completed a randomized, crossover study assessing the effects of short (4 h/night) and habitual (8 h/night) sleep duration on fasting and postprandial RMR and respiratory quotient (RQ). Measurements were taken after 3 nights using whole-room indirect calorimetry. The TEF was assessed over a 6-h period following consumption of a high-fat liquid meal. Results Short vs. habitual sleep did not affect RMR (1.01 ± 0.05 and 0.97 ± 0.04 kcal/min; p=0.23). Fasting RQ was significantly lower after short vs. habitual sleep (0.84 ± 0.01 and 0.88 ± 0.01; p=0.028). Postprandial EE (short: 1.13 ± 0.04 and habitual: 1.10 ± 0.04, p=0.09) and RQ (short: 0.88 ± 0.01 and habitual: 0.88 ± 0.01, p=0.50) after the high-fat meal were not different between conditions. TEF was similar between conditions (0.24 ± 0.02 kcal/min in both; p=0.98), as was the ~6-h incremental area under the curve (1.16 ± 0.10 and 1.17 ± 0.09 kcal/min x 356 min after short and habitual sleep, respectively; p=0.92). Conclusions Current findings observed in non-obese healthy premenopausal women do not support the hypothesis that alterations in TEF and postprandial substrate oxidation are major contributors to the higher rate of obesity observed in short sleepers. In exploring a role of sleep duration on EE, research should focus on potential alterations in physical activity to explain the increased obesity risk in short sleepers.

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