Abstract
Epidemiological studies have shown association of sleep disorders with adverse metabolic effects, including obesity, insulin resistance and type 2 diabetes mellitus in adults, with an increased risk of cardiometabolic disease and mortality. Categories of sleep disorders that contributed to the above diseases included changes in sleep duration, chronic sleep deprivation and excessive sleep, changes in sleep architecture, sleep fragmentation, circadian rhythm disorders (e.g., shift work), and obstructive sleep apnea syndrome. Sleep and circadian rhythms modulate or control daily physiological patterns, that play an important role for normal metabolic health. Various metabolic processes, including glucose tolerance, change during the day and night and at different stages of sleep. During sleep, the utilization of glucose by the brain and activity of the sympathetic nervous system decrease, and vagus nerve tone increases. Global rates of obesity and diabetes are on the rise worldwide, and the prevalence of sleep deprivation and sleep disorders are also on the rise. The results of epidemiological and pathophysiological studies conducted in different countries among the population of different socioeconomic groups confirm that sleep disorders predispose to a higher risk of cardiometabolic disorders, including type 2 diabetes. There is a bidirectional relationship between metabolic dysfunction and sleep disorders. Current research data suggest that sleep is a potentially modifiable risk factor for cardiometabolic disease and obesity. More clinical investigations are required to improve our understanding of the mechanisms underlying metabolic dysfunction associated with sleep disorders and to explore the potential benefit of normalizing sleep in people with metabolic disorders. Recommendations for the optimization and hygiene of sleep, treatment of sleep disorders, along with sufficient physical activity and proper nutrition, should be included in preventive and therapeutic strategies to maintain metabolic health.
Publisher
Publishing Company VIT-A-POL
Cited by
1 articles.
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