HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) CME questions Alert me when this article is cited Alert me if a correction is posted Permissions Request Permissions Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Lévy, P. Articles by Eckel, J. PubMed PubMed Citation Articles by Lévy, P. Articles by Eckel, J.

Sleep, sleep-disordered breathing and metabolic consequences

¹ INSERM ERI 17, HP2 laboratory, Joseph Fourier University and Sleep Laboratory, EFCR, Pôle Rééducation et Physiologie, CHU Grenoble, Grenoble, France, ² Dept of Medicine, Pneumology, Physiology and Nutrition (DIMPEFINU), University of Palermo, ³ Institute of Biomedicine and Molecular Immunology (IBIM), National Research Council (CNR), Palermo, Italy, and ⁴ German Diabetes Center, Düsseldorf, Germany.

CORRESPONDENCE: P. Lévy, EFCR, Pôle Rééducation et Physiologie, CHU Grenoble, BP 217, 38043 Cedex, France. E-mail: PLevy{at}chu-grenoble.fr

Keywords: Diabetes, insulin resistance, intermittent hypoxia, obesity, sleep, sleep apnoea

Received: November 5, 2008
Accepted February 25, 2009

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.

This article has been cited by other articles:

				P. Levy From the author: Eur. Respir. J., November 1, 2009; 34(5): 1210 - 1211. [Full Text] [PDF]

				P. Steiropoulos, N. Papanas, E. Maltezos, and D. Bouros Is there a metabolic effect of continuous positive airway pressure in sleep apnoea? Adherence should not be underestimated Eur. Respir. J., November 1, 2009; 34(5): 1209 - 1210. [Full Text] [PDF]