Sleep and Glucose Intolerance/Diabetes Mellitus

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The sleep state itself has modulatory effects on glucose homeostasis. Epidemiologic and experimental studies suggest that sleep loss and sleep disturbances are detrimental to metabolic function and may predispose to obesity or glucose intolerance. Apart from the common risk factor of obesity, increasing data also support that obstructive sleep apnea exerts independent adverse effects on glucose intolerance and diabetes mellitus, although definitive evidence is still needed.

Section snippets

Glucose metabolism and its clinical disorders

Diabetes mellitus is a group of metabolic disorders characterized by chronic hyperglycemia caused by various pathogenetic processes in glucose homeostasis [1], [2]. In health, glucose homeostasis is achieved by regulating glucose production by the liver (gluconeogenesis) and glucose use by insulin-dependent tissues, such as muscle and fat, and non–insulin-dependent tissues, such as the brain [3]. Insulin is secreted by pancreatic β cells, both constitutionally and acutely in response to glucose

Influence of sleep on glucose metabolism

Contrary to most mammals, human sleep is generally consolidated into a single 7- to 9-hour period, leading to an extended period of fasting overnight. Both pancreatic β-cell responsiveness and insulin sensitivity are influenced by sleep. Despite the extended fast during overnight sleep, blood glucose levels remain stable or fall only minimally. By comparison, when individuals are awake and fasting in a recumbent position without any physical activity, glucose levels decrease an average of 10 to

Sleep-disordered breathing and glucose metabolism

Obstructive sleep apnea (OSA) is the most common form of SDB worldwide [55], [56]. A high association between OSA and glucose intolerance/diabetes mellitus would not be unexpected because they share the common risk factor of obesity. Research momentum has focused on the hunt for evidence of independent pathogenetic links between SDB and glucose metabolism disorders. The identification of a causal role would have implications not only on the understanding of disease pathogenesis but also on

Summary

The sleep state itself has modulatory effects on glucose homeostasis. Epidemiologic and experimental studies suggest that sleep loss and sleep disturbances are detrimental to metabolic function and may predispose to obesity or glucose intolerance. Apart from the common risk factor of obesity, increasing data also support that OSA exerts independent adverse effects on glucose intolerance/diabetes mellitus, although definitive evidence is still needed.

Acknowledgments

The authors are grateful to Professor Eve Van Cauter of the University of Chicago for her support with the preparation of this manuscript.

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