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This study will test the hypothesis that a late sleep (Ls) and/or late meal (Lm) behavioral pattern, with equal sleep duration, will promote positive energy balance and insulin resistance (IR).
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Sleeping patterns affect aspects of metabolism that may impact obesity risk; our lab is interested in studying whether sleep patterns play a role in the development of obesity. Individuals with late bedtimes and late rise times tend to have greater food intake which includes more fast food and sugar-sweetened beverages, less fruits and vegetables [1], larger portions, and later eating times [2] than those with earlier bedtimes. This sleeping pattern is highly prevalent: ~15 million Americans work on shifts other than regular day hours [3] and others subject themselves to 'social jetlag' (time difference between the middle of the sleep episode [midpoint of sleep] on work days and non-work days, similar to travel across time zones) [4]. The shift in sleep and meal times associated with these lifestyles results in misalignment of sleep and eating behaviors with the circadian clocks. These clocks, located in the brain and organs throughout the body, regulate metabolism and behavior and are affected by sleep and feeding. Disruption of clock genes in individual organs may be in part responsible for metabolic dysregulation [5]. Altering the coordination of sleep and meal timing may affect food reward valuation (brain) and metabolism (peripheral organs) to promote obesity and IR, observed more frequently in shift workers. This is the focus of this randomized, crossover, controlled study of 4 phases:
Aim 2: To determine whether neuronal responses to food stimuli in brain regions related to reward value explain differences in food intake.
• Hypothesis 2: (a) Increased brain activity in response to visual presentation of food stimuli, using functional magnetic resonance imaging (fMRI), will be seen in Ls and Lm compared to Ns and Nm in the insula and the orbitofrontal cortex. Enhanced neuronal activity in response to foods will be most pronounced in the Ls/Lm phase (Ns/Nm<Ls/Nm≤Ns/Lm<Ls/Lm). (b) Neuronal responses to food stimuli will be related to pre-test neuropeptide Y (NPY), hypocretin-1, and subsequent food intake.
Exploratory Aim 3: To determine whether meal or sleep timing affect glucose homeostasis and appetite-regulating hormones.
• Hypothesis 3: Ls and Lm will result in lower insulin sensitivity (frequently sampled i.v. glucose tolerance test [FSIVGTT] and meal tolerance test [MTT]) than Ns and Nm (Ns/Nm>Ls/Nm≥Ns/Lm>Ls/Lm). Sleep and meal timing will have independent and interactive effects on the 24-h pattern of hormones regulating food intake (lower leptin and glucagon-like peptide-1 [GLP-1]; higher ghrelin, NPY and hypocretin-1).
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6 participants in 4 patient groups
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Data sourced from clinicaltrials.gov
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