title: Biological plausibility linking sleep apnoea and metabolic dysfunction.
abstract: Obstructive sleep apnoea (OSA) is a very common disorder that affects 10-25% of the general population. In the past two decades, OSA has emerged as a cardiometabolic risk factor in both paediatric and adult populations. OSA-induced metabolic perturbations include dyslipidaemia, atherogenesis, liver dysfunction and abnormal glucose metabolism. The mainstay of treatment for OSA is adenotonsillectomy in children and continuous positive airway pressure therapy in adults. Although these therapies are effective at resolving the sleep-disordered breathing component of OSA, they do not always produce beneficial effects on metabolic function. Thus, a deeper understanding of the underlying mechanisms by which OSA influences metabolic dysfunction might yield improved therapeutic approaches and outcomes. In this Review, we summarize the evidence obtained from animal models and studies of patients with OSA of potential mechanistic pathways linking the hallmarks of OSA (intermittent hypoxia and sleep fragmentation) with metabolic dysfunction. Special emphasis is given to adipose tissue dysfunction induced by sleep apnoea, which bears a striking resemblance to adipose dysfunction resulting from obesity. In addition, important gaps in current knowledge and promising lines of future investigation are identified.
authors.affiliation: Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, Knapp Center for Biomedical Discovery, Room 4100, 900 East 57th Street, Mailbox 4, Chicago, Illinois 60637-1470, USA.
authors.forename: Alex
authors.initials: A
authors.lastname: Gileles-Hillel
authors.affiliation: Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, Knapp Center for Biomedical Discovery, Room 4100, 900 East 57th Street, Mailbox 4, Chicago, Illinois 60637-1470, USA.
authors.forename: Leila
authors.initials: L
authors.lastname: Kheirandish-Gozal
authors.affiliation: Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, Knapp Center for Biomedical Discovery, Room 4100, 900 East 57th Street, Mailbox 4, Chicago, Illinois 60637-1470, USA.
authors.forename: David
authors.initials: D
authors.lastname: Gozal
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008659:Metabolic Diseases / Q000209:etiology* / Q000628:therapy; D012891:Sleep Apnea Syndromes / Q000150:complications* / Q000628:therapy