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. 2011 Jul;14(4):402-12.
doi: 10.1097/MCO.0b013e3283479109.

Sleep and Obesity

Free PMC article

Sleep and Obesity

Guglielmo Beccuti et al. Curr Opin Clin Nutr Metab Care. .
Free PMC article


Purpose of review: This review summarizes the most recent evidence linking decreased sleep duration and poor sleep quality to obesity, focusing upon studies in adults.

Recent findings: Published and unpublished health examination surveys and epidemiological studies suggest that the worldwide prevalence of obesity has doubled since 1980. In 2008, 1 in 10 adults was obese, with women more likely to be obese than men. This obesity epidemic has been paralleled by a trend of reduced sleep duration. Poor sleep quality, which leads to overall sleep loss has also become a frequent complaint. Growing evidence from both laboratory and epidemiological studies points to short sleep duration and poor sleep quality as new risk factors for the development of obesity.

Summary: Sleep is an important modulator of neuroendocrine function and glucose metabolism and sleep loss has been shown to result 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. Recent epidemiological and laboratory evidence confirm previous findings of an association between sleep loss and increased risk of obesity.


Figure 1
Figure 1. Main pathways connecting sleep–wake regulation and feeding and possible mechanisms for the adverse impact of sleep loss on energy homeostasis
Central to this hypothesis is the role of the orexin system, which is inhibited by sleep-promoting neurons in the ventrolateral preoptic area (VLPO) containing gamma-aminobutyric acid (GABA). The orexigenic neurons, located in the lateral hypothalamic area (LHA) and posterior hypothalamus (PH), play a major role in the maintenance of arousal by activating the ascending arousal system and the entire cerebral cortex and modulating other central nervous system nuclei and structures involved in sleep–wake regulation. Orexin activity is also involved in the regulation of feeding by: (a) increasing the activity of the neuropeptide Y (NPY) neurons in the arcuate nucleus of the hypothalamus, thus, affecting homeostatic food intake; (b) stimulating the nucleus tractus solitarius (NTS) and the paraventricular nucleus (PVN), which integrate peripheral signals of energy balance, appetite, and satiety; (c) stimulating the dopaminergic ventrotegmental area (VTA) and nucleus accumbens (NA), the ‘reward centers’, which regulate nonhomeostatic food intake; (d) increasing sympathetic activity, which will in turn inhibit leptin release and stimulate ghrelin release. Lower leptin and higher ghrelin levels will act in concert to further activate orexin neurons resulting in an increased drive for both homeostatic and nonhomeostatic food intake. Adapted with permission from [11].

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