Chronic high‐caloric diet modifies sleep homeostasis in mice

Abstract

Obesity prevalence and sleep habit changes are commonplace nowadays, due to modern lifestyle. A bidirectional relationship likely exists between sleep quality and metabolic disruptions, which could impact quality of life. In our study, we investigated the effects of a chronic high-caloric diet on sleep architecture and sleep regulation in mice. We studied the effect of 3 months high-caloric diet (HCD, 45% fat) on sleep and the sleep electroencephalogram (EEG) in C57BL/6J mice during 24-hr baseline (BL) recordings, and after 6-hr sleep deprivation (SD). We examined the effect of HCD on sleep homeostasis, by performing parameter estimation analysis and simulations of the sleep homeostatic Process S, a measure of sleep pressure, which is reflected in the non-rapid-eye-movement (NREM) sleep slow-wave-activity (SWA, EEG power density between 0.5 and 4.0 Hz). Compared to controls (n = 11, 30.7 ± 0.8 g), mice fed with HCD (n = 9, 47.6 ± 0.8 g) showed an increased likelihood of consecutive NREM-REM sleep cycles, increased REM sleep and decreased NREM sleep EEG SWA. After SD, these effects were more pronounced. The simulation resulted in a close fit between the time course of SWA and Process S in both groups. HCD fed mice had a slower time constant (T = 15.98 hr) for the increase in homeostatic sleep pressure compared with controls (5.95 hr) indicating a reduced effect of waking on the increase in sleep pressure. Our results suggest that chronic HCD consumption impacts sleep regulation.

Sleep Network Deterioration as a Function of Dim-Light-At-Night Exposure Duration in a Mouse Model

“…Subsequently, a 24-h light-dark period was recorded (control LD), starting at lights on, followed by 12-h light and 12-h DLAN (acute DLAN, 1d DLAN ) (schematic overview of experimental design in Figure 1 a). For the four experimental conditions, namely 1d DLAN, 1w DLAN, 1m DLAN , and 3m DLAN , first a baseline day (BL, 12L:12DLAN) was recorded, followed by a second day in the same light/DLAN schedule, at the start of which six hours of sleep deprivation were conducted by gentle handling [ 22 , 23 , 24 , 30 ]. EEG and EMG were recorded continuously during BL and sleep deprivation, as well as for 18 h of recovery period.…”

“…Before the start of the EEG and electromyogram (EMG) recordings (1-2 weeks approximately), under deep anesthesia (Ketamine 100 mg/kg; Xylazine 10 mg/kg; Atropine 1 mg/kg), EEG recording screws (placed above the somatosensory cortex and cerebellum) and EMG electrodes (placed on the neck muscle) (Plastics One, Roanoke, VA, USA) were implanted as described previously [22][23][24][25]. The wire branches of all electrodes were set in a plastic pedestal (Plastics One, Roanoke, VA, USA) and fixed to the skull with dental cement.…”

“…The EEG and EMG were recorded with a portable recording system (PS 1 system, Institute of Pharmacology and Toxicology, Zurich, Switzerland) as previously described [22][23][24][25]29]. Before each recording, a calibration signal was recorded on the EEG and EMG channels.…”

“…Three vigilance states (Waking, NREM sleep, and REM sleep) were scored offline in 4 s epochs by visual inspection of the EEG and EMG signals as well as EEG power density in the slow-wave range, as described previously [22][23][24]30]. For each epoch, the EEG power density in the delta (0.75-4.0 Hz) and theta band (6.25-9.0 Hz) and the integrated EMG value were graphically displayed on a PC monitor to enable scoring of the different vigilance states.…”

“…In order to test the sleep homeostatic response after elevated sleep pressure, we conducted a 6-h sleep deprivation in all DLAN groups [22][23][24][25]30]. Sleep deprivation induced differences among DLAN groups, separating the 3m DLAN from the other groups, the latter showing more waking and less NREM, during the light period following the sleep deprivation (Figure 3, Figure 5 and Figure S4).…”