There is emerging evidence in the literature to suggest that disruption of the normal circadian rhythm (sleep–wake cycle signalling) is a potential risk factor to explain the increased incidence of metabolic syndrome. Over the last century, obesity, diabetes and other components of metabolic syndrome have been on the rise. On the other hand, the amount of sleep has decreased from an average of 6–8 h per night. Furthermore, the quality of sleep has declined with more individuals voluntarily decreasing their amount of sleep to work or enjoy leisure activities. Over the last decade, researchers have examined the relationship between disruption in human circadian system and the emergence of symptoms related to metabolic syndrome. Indeed, epidemiological studies suggest a relation between sleep duration and diabetes and obesity. Moreover, experimental animal and human studies suggest such a relation. These studies propose optimum sleep duration of 7–8 h per night to avoid circadian rhythm disruption and suggest that sleep disturbance, whether iatrogenic or disease-related, should be considered as a risk factor for metabolic syndrome, and be addressed. This field is in its infancy and further understanding of specific pathophysiological pathways of circadian desynchronisation will help in developing novel preventive and therapeutic strategies.
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