![]() Deep non-REM sleep is characterized by ‘slow waves’ in the electroencephalogram (EEG), which reflect a mode of synchronous firing of thalamo-cortical neurons. ![]() Human sleep is comprised of rapid-eye-movement (REM) sleep and non-REM sleep. The molecular and neuronal mechanisms that measure the duration of prior wakefulness and are thus responsible for the homeo-static control of sleep have not been fully elucidated. Circadian timing is transmitted to other areas of the brain and to the periphery via direct neuronal connections with other parts of the hypothalamus, via the control of sympathetic nervous activity and via hormonal signals, including melatonin. The generation and maintenance of circadian oscillations in SCN neurons involve a series of clock genes (including at least per1, per 2, per3, cry1, cry2, tim, clock, B-mal1, CKIε/δ), often referred to as ‘canonical’, which interact in a complex feedback loop of transcription/translation. Instead, single SCN cells in culture can generate circadian neural signals. The ability of the SCN nuclei to generate a circadian signal is not dependent on cell-to-cell interaction and synchronization. a measure of the duration of prior wakefulness, irrespective of time of day).Ĭircadian rhythmicity is an endogenous oscillation with a near 24-hour period generated in the suprachiasmatic nuclei of the hypothalamus. intrinsic effects of biological time, irrespective of the sleep or wake state) and sleep-wake homeostasis (i.e. Sleep propensity and sleep architecture are in turn controlled by the interaction of two time-keeping mechanisms in the central nervous system, circadian rhythmicity (i.e. Glucose tolerance and insulin secretion are also markedly modulated by the sleep-wake cycle. The temporal organization of the release of the counterregulatory hormones growth hormone (GH) and cortisol as well as the release of hormones that play a major role in appetite regulation, such as leptin and ghrelin, is partly dependent on sleep timing, duration and quality. Hormones that Influence Glucose Regulation and Appetite Control Are Influenced by Sleep Avoiding sleep deprivation may help to prevent the development of obesity, particularly in children. Bedtime extension in short sleepers should be explored as a novel behavioral intervention that may prevent weight gain or facilitate weight loss. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity. The present chapter reviews epidemiologic studies in adults and children and laboratory studies in young adults indicating that sleep restriction results in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin and increased hunger and appetite. Accumulating evidence from both epidemiologic studies and well-controlled laboratory studies indicates that chronic partial sleep loss may increase the risk of obesity and weight gain. ![]() Evidence that the curtailment of sleep duration may have adverse health effects has emerged in the past 10 years. ![]() However, sleep plays a major role in neuroendocrine function and glucose metabolism. Sleeping as little as possible is often seen as an admirable behavior in contemporary society. Compared to a few decades ago, adults, as well as children, sleep less.
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