Abstract
Nutritional state in the gestation period influences fetal growth and development. We hypothesized that undernutrition during gestation would affect offspring sleep architecture and/or homeostasis. Pregnant female mice were assigned to either control (fed ad libitum; AD) or 50% dietary restriction (DR) groups from gestation day 12 to parturition. After parturition, dams were fed AD chow. After weaning, the pups were also fed AD into adulthood. At adulthood (aged 8–9 weeks), we carried out sleep recordings. Although offspring mice displayed a significantly reduced body weight at birth, their weights recovered three days after birth. Enhancement of electroencephalogram (EEG) slow wave activity (SWA) during non-rapid eye movement (NREM) sleep was observed in the DR mice over a 24-hour period without changing the diurnal pattern or amounts of wake, NREM, or rapid eye movement (REM) sleep. In addition, DR mice also displayed an enhancement of EEG-SWA rebound after a 6-hour sleep deprivation and a higher threshold for waking in the face of external stimuli. DR adult offspring mice exhibited small but significant increases in the expression of hypothalamic peroxisome proliferator-activated receptor α (Pparα) and brain-specific carnitine palmitoyltransferase 1 (Cpt1c) mRNA, two genes involved in lipid metabolism. Undernutrition during pregnancy may influence sleep homeostasis, with offspring exhibiting greater sleep pressure.
Highlights
Timing, duration, and depth of sleep are controlled by the interaction of the time of day and by the duration of prior wakefulness [1,2,3]
We found in this study for the first time that sleep homeostasis is affected by prenatal nutritional condition
Our dietary restriction (DR) adult offspring mice born with Low birth weight (LBW) showed an enhancement of slow wave activity (SWA) during non-rapid eye movement (NREM) sleep, which is accepted to be a parameter of sleep pressure or sleep intensity
Summary
Duration, and depth of sleep are controlled by the interaction of the time of day (circadian control) and by the duration of prior wakefulness (homeostatic control) [1,2,3]. It has been demonstrated that metabolic function, including adenosine regulation, is critically involved in sleep homeostasis [7,8,9]. It has been reported that peroxisome proliferator-activated receptors (PPARs) and AMP-activated protein kinase (AMPK) play key roles in the regulation of sleep homeostasis [10,11]. PPARs are transcription factors belonging to the nuclear receptor family, and are closely related to the regulation of lipid metabolism [12,13,14]. AMPK acts as an efficient sensor of cellular energy states regulating glucose and lipid metabolism [15,16,17]. In addition to PPARs, AMPK activity changes SWA without affecting sleep duration [11]
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