Metabolic consequences of sleep and circadian disorders

Abstract

Sleep and circadian rhythms modulate or control daily physiological patterns with importance for normal metabolic health. Sleep deficiencies associated with insufficient sleep schedules, insomnia with short-sleep duration, sleep apnea, narcolepsy, circadian misalignment, shift work, night eating syndrome, and sleep-related eating disorder may all contribute to metabolic dysregulation. Sleep deficiencies and circadian disruption associated with metabolic dysregulation may contribute to weight gain, obesity, and type 2 diabetes potentially by altering timing and amount of food intake, disrupting energy balance, inflammation, impairing glucose tolerance, and insulin sensitivity. Given the rapidly increasing prevalence of metabolic diseases, it is important to recognize the role of sleep and circadian disruption in the development, progression, and morbidity of metabolic disease. Some findings indicate sleep treatments and countermeasures improve metabolic health, but future clinical research investigating prevention and treatment of chronic metabolic disorders through treatment of sleep and circadian disruption is needed.

Figure 1

Model of the hypothesized relationships between sleep and circadian disorders and type 2 diabetes. Sleep deficiency can result from several sleep and circadian disorders including insufficient sleep, periodic limb movement disorder (PLMD), insomnia and narcolepsy. By working at times that overlap with the normal sleep opportunity, shift work and shiftwork disorder can induce circadian misalignment contributing to sleep deficiency. There is a bidirectional relationship between obesity and sleep apnea and apnea results in both hypoxemia and sleep deficiency. Sleep deficiency is also associated with increased risk of obesity. Sleep deficiency, circadian misalignment, obesity and hypoxia are associated with increased inflammation, oxidative stress, impaired glucose tolerance and insulin resistance. Thus, sleep problems likely increase type 2 diabetes risk through multiple pathways.