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Sleep, sleep-disordered breathing and metabolic consequences

Published on Jul 1, 2009in European Respiratory Journal11.807
· DOI :10.1183/09031936.00166808
Patrick Levy60
Estimated H-index: 60
,
Marisa Bonsignore37
Estimated H-index: 37
,
J. Eckel3
Estimated H-index: 3
Sources
Abstract
Sleep profoundly affects metabolic pathways. In healthy subjects, experimental sleep restriction caused insulin resistance (IR) and increased evening cortisol and sympathetic activation. Increased obesity in subjects reporting short sleep duration leads to speculation that, during recent decades, decreased sleeping time in the general population may have contributed to the increasing prevalence of obesity. Causal inference is difficult due to lack of control for confounders and inconsistent evidence of temporal sequence. In the general population, obstructive sleep apnoea (OSA) is associated with glucose intolerance. OSA severity is also associated with the degree of IR. However, OSA at baseline does not seem to significantly predict the development of diabetes. Prevalence of the metabolic syndrome is higher in patients with OSA than in obese subjects without OSA. Treatment with continuous positive airway pressure seems to improve glucose metabolism both in diabetic and nondiabetic OSA but mainly in nonobese subjects. The relative role of obesity and OSA in the pathogenesis of metabolic alterations is still unclear and is intensively studied in clinical and experimental models. In the intermittent hypoxia model in rodents, strong interactions are likely to occur between haemodynamic alterations, systemic inflammation and metabolic changes, modulated by genetic background. Molecular and cellular mechanisms are currently being investigated.
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References193
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There is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways. The development of translational models of intermittent hypoxia has allowed investigation of its role in the activation of inflammatory mechanisms and promotion of cardiovascular disease in OSAS. There are noticeable differences in the response to intermittent hypoxia between body tissues but the...
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Introduction The aim of this retrospective study was to investigate if sleep-disordered breathing (SDB) was an independent predictor of suspected fatty liver disease in a clinical sample of overweight children and adolescents.
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Sleep-disordered breathing is highly prevalent in childhood obesity. Two recent cross-sectional studies have demonstrated an independent association between the severity of sleep-disordered breathing and the metabolic syndrome. A limited number of studies have also addressed the correlation between sleep-disordered breathing and insulin resistance, the core factor of the metabolic syndrome. Cross-sectional reports in modestly obese children are in favor of an association between sleep apnea and ...
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Obstructive sleep apnea (OSA) and type 2 diabetes mellitus are frequently comorbid conditions. Clinic-based estimates of the prevalence of OSA in type 2 diabetics range from 18% to as high as 36%,1–3 and some 50% of patients with OSA have type 2 diabetes or impaired carbohydrate metabolism.4 Population surveys, the Wisconsin Sleep Cohort,5 and the Sleep Heart Health Study6 estimate the prevalence of type 2 diabetes in patients with OSA (apnea-hypopnea index [AHI] > 15) to be about 15%. Obesity i...
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The prevalence of childhood obesity is increasing worldwide. One of the obesity-related complications that has received increasing attention in recent years is sleep-disordered breathing. Obese children are at a higher risk of developing sleep-disordered breathing, including habitual snoring, obstructive sleep apnea syndrome and desaturations preceded by central apneas. Both adiposity and upper airway factors, such as adenotonsillar hypertrophy, modulate the severity of sleep-disordered breathin...
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