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    • Sleep deprivation seems to be related to the

    2018-10-26

    Sleep deprivation seems to be related to the elevation of cortisol, reflecting impairment of HPA axis regulation, and resulting in glucocorticoid overload, which can lead to large deleterious effects on the body. Moreover, there is an association between short sleep duration and higher risk of developing obesity and type II diabetes, suggesting the HPA axis hyperactivation as one of the mechanism involved in the metabolic consequences of sleep loss [33,34].
    Effects of glucocorticoids on sleep and metabolism Classic studies in rats and humans have demonstrated that exogenous CRH is able to modulate sleep by increasing EEG frequency and wakefulness and decreasing SWS [35,36]. However, studies focused on the direct effects of glucocorticoids have shown that they increase time spent awake at the expense of REM sleep [37]. Other studies show that parp inhibitors decreases SWS when MRs are activated, while dexamethasone increases awakening after activation of GRs [38]. The effects of both exogenous and endogenous glucocorticoids on sleep EEG depend on the type and location of the receptors activated (MR vs. GR), the dose of cortisol/corticosterone used, and the optimal cortisol levels to effect maximal nocturnal CRH suppression [4,39]. Studies that have demonstrated decreases in SWS with elevated cortisol levels and total occupation of GR may be due to excessive GR activation in the amygdala. The effects are opposite to the known inhibitory action found in PVN and anterior pituitary, leading to positive feedback [39,40]. However, the effects of glucocorticoids as well as CRH on REM are not well understood and most of them are contradictory [4]. Chronic exposure to excess glucocorticoids, such as occurs during diseases like Cushing׳s syndrome, can offer insight into the role of these hormones in sleep. For example, consistent alterations in polysomnographic recordings are reported in Cushing׳s syndrome, such as reduction of SWS, increased sleep latency, enhanced wake time, shortened REM latency, and elevated REM density, among others [17], reflecting the deleterious effects of glucocorticoid excess. Bierwolf and colleagues [41] have demonstrated that adrenal secretory activity starts predominantly during periods of NREM in both Cushing׳s and healthy patients, showing a link between pituitary–adrenal activity and the ultradian rhythmicity of NREM and REM sleep. Reductions in sleep duration have become common due to the socioeconomic demands and opportunities in modern society [42]. In average, self-reported sleep time has decreased 1.5–2h in the USA [43]. Quantitative alterations in sleep duration may impact the metabolic balance of the body, including control of body mass and food intake, glucose metabolism, and adipokine levels (for review, see [44]). In addition to the neurocognitive consequences of sleep loss, recent studies have been focused on the role of sleep in areas outside the brain, including other organs and physiological systems, such as the metabolism [45]. Many studies have shown an association between sleep duration and obesity both in adults and children, suggesting that short sleep duration may be a predictor of weight gain [46–48] and an important risk factor for development of insulin resistance, diabetes, and cardiovascular disease [16,49,50]. A meta-analysis revealed that each reduction of 1h of sleep per day is associated with an increase of 0.35kgm−2 in body mass index (BMI) [51]. These observed changes due to sleep loss indicate a probable imbalance between food intake and energy expenditure caused by neuroendocrine alterations. Naturally, sleep is a period of fasting. Glucose utilization by the brain is increased during REM sleep at the end of the night [52], leading to a negative energy balance in the body. However, sleep “resets” the metabolism and energy expenditure rates in the brain, giving effective and flexible control of energy expenditure under changing environmental pressures [53]. Much like sleep, hypothalamic control of metabolism is comprised by mutually inhibiting networks. The appetite-promoting neuropeptide Y (NPY) and agouti-related protein (AGRP) neurons mutually inhibit the appetite-suppressing pro-opiomelanocortin (POMC) and amphetamine-related transcript (CART) neurons. Both sets of neurons work as sensors of the circulating hormones leptin and ghrelin. Leptin is produced by adipose tissues and promotes satiety through inhibition of NPY/AGRP neurons and activation of POMC/CART neurons, with higher levels during sleep compared to awake states, independent of food intake [54]. Recent animal studies have also suggested that leptin participates in sleep regulation, reducing REM sleep and modulating SWS [55]. In turn, ghrelin is an appetite-stimulating hormone produced in the gut, which acts by inhibiting POMC/CART and activating NPY/AGRP. Like leptin, ghrelin has higher levels during sleep, which are followed by a decrease in the morning before the breakfast [56]. Current evidence indicates that ghrelin is also a sleep-promoting factor, able to induce SWS and stimulates GH secretion during the night [57,58].