Sleep and eating in childhood: a potential behavioral mechanism underlying the relationship between poor sleep and obesity.

OBJECTIVE: The goal of our study was to examine the associations between sleep and eating behaviors. Specifically, we examined associations between sleep duration and continuity with behaviors that promote eating regardless of true physiologic hunger state including emotional (food intake in response to emotional distress) external (eating in response to the sight or smell of food), and restrained eating (a paradoxical behavior; food intake is initially reduced to lose or maintain body weight, but followed by increased consumption and binge eating). PARTICIPANTS: Fifty-six children (29 boys; 27 girls) ages 5 to 12 years participated in the study. Mean age was 7.7±1.9 years, and average body mass index (BMI) was within the healthy range (17.8±4.3 kg/m(2)). METHODS: Sleep duration, continuity and schedule were assessed using actigraphy and self-reports. The Child Dutch Eating Behavior Questionnaire-modified version (DEBQ-M) was used to examine levels of emotional, external and restrained eating in the children. RESULTS: Associations between the sleep and eating behaviors were examined using partial correlations and multiple regression analyses. External eating score was negatively associated with sleep duration; emotional eating score was associated with lower levels of sleep continuity; and restrained eating score were associated with a later sleep start and later bedtime. CONCLUSIONS: Short sleep duration and poor sleep continuity were associated with higher levels of eating behaviors shown to be associated with increased food intake. Therefore, sleep loss may be associated with diminished self-regulation of appetite in children, increasing the risk for overeating and obesity.

Nociceptin induces hypophagia in the perifornical and lateral hypothalamic area.

Nociceptin/orphanin FQ (N/OFQ) is known to induce food intake when administered into the lateral ventricle or certain brain areas. This is somewhat contradictory to its reward-suppressing role, as food is a strong rewarding stimulus. This discrepancy may be due to the functional diversity of N/OFQ's target brain areas. N/OFQ has been shown to inhibit orexin and melanin-concentrating hormone (MCH) neurons, both of which are appetite-inducing cells. As the expression of these neurons is largely confined to the lateral hypothalamus/perifornical area (LH/PFA), we hypothesized that N/OFQ inhibits food intake by acting in this area. To test this hypothesis, we examined the effect of local N/OFQ infusion within the LH/PFA on food intake in the rat and found that N/OFQ decreased sugar pellet as well as chow intake. This effect was not seen when the injection site was outside of the LH/PFA, suggesting a site-specific effect. Next, to determine a possible cellular mechanism of N/OFQ action on food intake, whole cell patch clamp recordings were performed on rat orexin neurons. As previously reported in mice, N/OFQ induced a strong and long lasting hyperpolarization. Pharmacological study indicated that N/OFQ directly inhibited orexin neurons by activating ATP-sensitive potassium (KATP) channels. This effect was partially but significantly attenuated by the inhibitors of PI3K, PKC and PKA, suggesting that the N/OFQ signaling is mediated by these protein kinases. In summary, our results demonstrate a KATP channel-dependent N/OFQ signaling and that N/OFQ is a site-specific anorexic peptide.

Local network regulation of orexin neurons in the lateral hypothalamus.

Obesity and inadequate sleep are among the most common causes of health problems in modern society. Thus, the discovery that orexin (hypocretin) neurons play a pivotal role in sleep/wake regulation, energy balance, and consummatory behaviors has sparked immense interest in understanding the regulatory mechanisms of these neurons. The local network consisting of neurons and astrocytes within the lateral hypothalamus and perifornical area (LH/PFA), where orexin neurons reside, shapes the output of orexin neurons and the LH/PFA. Orexin neurons not only send projections to remote brain areas but also contribute to the local network where they release multiple neurotransmitters to modulate its activity. These neurotransmitters have opposing actions, whose balance is determined by the amount released and postsynaptic receptor desensitization. Modulation and negative feedback regulation of excitatory glutamatergic inputs as well as release of astrocyte-derived factors, such as lactate and ATP, can also affect the excitability of orexin neurons. Furthermore, distinct populations of LH/PFA neurons express neurotransmitters with known electrophysiological actions on orexin neurons, such as melanin-concentrating hormone, corticotropin-releasing factor, thyrotropin-releasing hormone, neurotensin, and GABA. These LH/PFA-specific mechanisms may be important for fine tuning the firing activity of orexin neurons to maintain optimal levels of prolonged output to sustain wakefulness and stimulate consummatory behaviors. Building on these exciting findings should shed further light onto the cellular mechanisms of energy balance and sleep-wake regulation.