Chronobiology and Obesity by Marta Garaulet & Jose M. Ordovás

Author:Marta Garaulet & Jose M. Ordovás
Language: eng
Format: epub
Publisher: Springer New York, New York, NY

Sleep and Glucose Metabolism

Blood glucose regulation is a tightly controlled physiological process. Both hypo- and hyperglycemia can have life-threatening consequences. The insulin signaling pathway plays a major role in regulating peripheral blood glucose levels. After a meal, blood glucose rises rapidly. Pancreatic beta cells respond to elevated glucose by releasing insulin to the blood stream, which promotes glucose uptake and utilization by insulin-sensitive organs such as liver, adipose tissues, and skeletal muscle. Insulin also inhibits glucogenic processes such as gluconeogenesis, lipolysis, and proteolysis. Insufficient insulin production from pancreatic beta cells or defects of the responsiveness of insulin-dependent target organs, a condition known as insulin resistance, causes glucose intolerance or diabetes [45]. In healthy individuals, glucose tolerance displays a circadian variation, which is higher in the evening than in the morning and reaches its nadir around midnight [46]. Interestingly, the timing of this midnight dip in glucose tolerance coincides with the occurrence of NREM sleep. A reduction in glucose utilization by the brain and the periphery during NREM sleep has been proposed as the cause of this rhythm [46]. One of the earliest experiments conducted by Kuhn et al. that linked sleep loss to compromised glucose metabolism involved subjecting healthy subjects to total sleep deprivation for 72–126 h [47]. These individuals showed a marked reduction in glucose tolerance throughout the testing period. While complete sleep deprivation is not common in humans, the more real life-related recurrent partial sleep restriction has also been shown to have an impact in glucose metabolism. A pilot laboratory study conducted by Spiegel et al. found that healthy young male subjects after being subjected to a sleep restriction protocol with a bedtime period reduced to 4 h per night for 6 days showed a 40% reduction in glucose tolerance [48]. Along the impaired glucose metabolism sleep-restricted subjects showed a reduced acute insulin response to glucose stimulation and reduced insulin sensitivity [48]. A more recent laboratory study revealed that even milder recurrent sleep restriction with 5.5 h of sleep per night negatively impacts on glucose tolerance and insulin sensitivity [49]. A negative effect of voluntary sleep curtailment on glucose metabolism has been reported in a number of large scale cross-sectional epidemiologic studies, carried out in several industrialized countries worldwide (reviewed in [41, 49]). These studies generally conclude that insufficient sleep predisposes individuals to glucose intolerance and increases the risk of developing diabetes, even after controlling for several covariants such as age, body mass index (BMI) and physical activity. Interestingly, some studies report a U-shaped relationship between sleep duration and glucose intolerance. Sleep of more than 8 h per night also associates with a higher risk of developing diabetes and may even impact negatively on life expectancy [41].

Not only is the duration of sleep important for proper glucose metabolism, but so is its quality. Slow Wave Sleep (SWS) has been proposed to be the most restorative among different stages of sleep in humans [50]. Reduced SWS is observed in elderly [51] and obese individuals [52, 53], and both groups are more vulnerable to develop T2D [54].

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