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    • Sleep curtailment is able to change

    2018-11-01

    Sleep curtailment is able to change food intake as a result of decreased secretion of leptin [59–61] and increased secretion of ghrelin [49,59,62], which leads to increased food intake [49]. Two consecutive nights of sleep restriction (4h of time in bed) in young men were associated with a 28% increase in ghrelin and 18% reduction in leptin during the day, leading to increased hunger (24%) and appetite (23%), mostly for energy-rich foods with high carbohydrate content and low nutritional quality, such as sweets, salty snacks and starchy foods [49]. Six consecutive nights of sleep restriction (4h of time in bed) increased sympathetic nervous system activity, evening thymidine phosphorylase inhibitor level and growth hormone, in addition to decreasing glucose effectiveness and the acute insulin response by 30% each, much like is found in non-insulin-dependent diabetes [16]. Buxton and colleagues [63] found that sleep restriction (5h/night) for 1 week significantly reduced insulin sensitivity, although no correlation was observed with cortisol levels. In a protocol of 14 consecutive days of sleep restriction (5.5h of time in bed) with ad libitum food intake, caloric consumption was increased during the night, when the individual would generally be sleeping, explaining in part the increased vulnerability for weight gain induced by sleep loss [64]. On the other hand, another study did not find differences in hunger ratings after 1 night of total sleep deprivation compared to 1 night of sleep recovery (8h time in bed) both in men and women [65]. However, actual food intake was not measured in this study, and therefore it is unknown whether participants would or would not have actually increased their food intake during the day of total sleep deprivation compared to the day of sleep rebound [66]. Gonnissen and colleagues [67] evaluated the effect of sleep fragmentation during 8h on subjective feelings of appetite in men. They did not find a significant reduction in total sleep duration, but rather a reduction in REM sleep and an increase in N2 sleep stage. The volunteers reported a greater desire to eat after the night of sleep fragmentation, suggesting that sleep quality may be more important than sleep duration for appetite regulation, although they did not measure food intake in this study [67]. Increasing specific clinical evidence has shown that sleep quality and metabolic-related systems are connected. For instance, 50–98% of patients with OSA are morbidly obese [6]. There is an association between OSA and type 2 diabetes [68]. Cross-sectional studies indicate that up to 30% of patients with OSA also present type 2 diabetes, while up to 86% of obese patients with type 2 diabetes have OSA [69,70]. Strong evidence suggests that OSA may increase the risk of developing insulin resistance, glucose intolerance and diabetes [71]. Metabolic disorders and OSA share common pathogenic pathways, such as alterations in autonomic nervous system regulation, increased inflammatory activity, alterations in adipokine levels and endothelial dysfunction, which may be involved in the interplay between these conditions [71]. However, it is not well understood whether these effects are likely due to obesity. In this sense, a systematic review showed that the current literature does not support the hypothesis that OSA independently influences glucose metabolism [72]. The methodological quality varied a lot within the included studies, pointing to a need for more powerful, long-term randomized controlled trials defining changes of insulin resistance as primary endpoint [72]. Obesity is commonly associated with narcolepsy, a sleep disorder characterized by hypocretin (also called orexin) deficiency, excessive daytime sleepiness, and frequent sleep attacks during the day [73]. Narcoleptic patients often present an excess of fat storage in abdominal depots, metabolic alterations, and craving for food with a binge eating pattern [74,75]. The responsiveness of orexin neurons to peripheral metabolic cues, such as leptin and glucose, and the dopaminergic reward system response suggest that both of these 2 neurons are related to the regulation of energy homeostasis and vigilance states [76]. The studies are limited and it is not clear if narcolepsy independently affects glucose metabolism. A recent case-control study showed no clinically relevant pathologic findings in the glucose metabolism of narcoleptic patients compared to weight matched controls [77]. On the other hand, Poli and colleagues showed that narcoleptic patients have higher BMIs and BMI-independent metabolic alterations, such as higher waist circumference, high-density lipoprotein cholesterol, and insulin resistance, compared to idiopathic hypersomnia patients [78]. Evidence has shown that continuous disruption of circadian rhythm in human shift workers is associated with weight gain, metabolic disturbances, type 2 diabetes, and cardiovascular diseases due to increases in postprandial glucose, insulin, cortisol, and mean arterial pressure and decreased 24h leptin levels [45,79,80].