The diurnal variation of the geophysical position of the earth in relation to the sun has imposed considerable evolutionary pressure. The suprachiasmatic nucleus, which serves as the central biological clock, receives the input regarding light-dark through the optic nerves. This nucleus in turn conveys output in a diurnal fashion to other hypothalamic nuclei and to the autonomic nervous system. Sleep is the most extreme phenotypical adaptation to this diurnal light-dark cycle. In recent years, sleep duration has been reduced and sleep deprivation has become endemic in our modern 24/7 society, either by voluntary sleep restriction and/or through sleep disorders. Experimental studies in humans have documented that sleep deprivation induces insulin resistance in multiple metabolic pathways in both healthy subjects and patients with type 1 diabetes. Epidemiological studies have documented that sleep duration is an important risk factor for development of insulin resistance and type 2 diabetes. Several potential pathways have been suggested to contribute to insulin resistance after sleep restriction, including altered function of the autonomic nervous system, endocrine changes, and an altered inflammatory state. Nonetheless, the causal factors explaining the relation between altered sleep characteristics and insulin resistance in multiple organs need additional study, and most likely include central autonomic pathways.
Keywords: Biological clock; insulin resistance; sleep deprivation; sleep disorders; type 1 diabetes; type 2 diabetes.
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