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Article: Obesity, obstructive sleep apnoea and metabolic syndrome

TitleObesity, obstructive sleep apnoea and metabolic syndrome
Authors
Issue Date2012
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/RES
Citation
Respirology, 2012, v. 17 n. 2, p. 223-236 How to Cite?
AbstractOSA is increasingly recognized as a major health problem in developed countries. Obesity is the most common risk factor in OSA and hence, the prevalence of OSA is undoubtedly rising given the epidemic of obesity. Recent data also suggest that OSA is highly associated with the metabolic syndrome, and it is postulated that OSA contributes to cardiometabolic dysfunction, and subsequently vasculopathy. Current evidence regarding the magnitude of impact on ultimate cardiovascular morbidity or mortality attributable to OSA-induced metabolic dysregulation is scarce. Given the known pathophysiological triggers of intermittent hypoxia and sleep fragmentation in OSA, the potential mechanisms of OSA-obesity-metabolic syndrome interaction involve sympathetic activation, oxidative stress, inflammation and neurohumoral changes. There is accumulating evidence from human and animal/cell models of intermittent hypoxia to map out these mechanistic pathways. In spite of support for an independent role of OSA in the contribution towards metabolic dysfunction, a healthy diet and appropriate lifestyle modifications towards better control of metabolic function are equally important as CPAP treatment in the holistic management of OSA. © 2011 Asian Pacific Society of Respirology.
Persistent Identifierhttp://hdl.handle.net/10722/163450
ISSN
2015 Impact Factor: 3.078
2015 SCImago Journal Rankings: 1.157
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLam, JCMen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorIp, MSMen_US
dc.date.accessioned2012-09-05T05:31:32Z-
dc.date.available2012-09-05T05:31:32Z-
dc.date.issued2012en_US
dc.identifier.citationRespirology, 2012, v. 17 n. 2, p. 223-236en_US
dc.identifier.issn1323-7799en_US
dc.identifier.urihttp://hdl.handle.net/10722/163450-
dc.description.abstractOSA is increasingly recognized as a major health problem in developed countries. Obesity is the most common risk factor in OSA and hence, the prevalence of OSA is undoubtedly rising given the epidemic of obesity. Recent data also suggest that OSA is highly associated with the metabolic syndrome, and it is postulated that OSA contributes to cardiometabolic dysfunction, and subsequently vasculopathy. Current evidence regarding the magnitude of impact on ultimate cardiovascular morbidity or mortality attributable to OSA-induced metabolic dysregulation is scarce. Given the known pathophysiological triggers of intermittent hypoxia and sleep fragmentation in OSA, the potential mechanisms of OSA-obesity-metabolic syndrome interaction involve sympathetic activation, oxidative stress, inflammation and neurohumoral changes. There is accumulating evidence from human and animal/cell models of intermittent hypoxia to map out these mechanistic pathways. In spite of support for an independent role of OSA in the contribution towards metabolic dysfunction, a healthy diet and appropriate lifestyle modifications towards better control of metabolic function are equally important as CPAP treatment in the holistic management of OSA. © 2011 Asian Pacific Society of Respirology.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/RESen_US
dc.relation.ispartofRespirologyen_US
dc.titleObesity, obstructive sleep apnoea and metabolic syndromeen_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1440-1843.2011.02081.xen_US
dc.identifier.pmid21992649-
dc.identifier.scopuseid_2-s2.0-84856240103en_US
dc.identifier.volume17en_US
dc.identifier.issue2en_US
dc.identifier.spage223en_US
dc.identifier.epage236en_US
dc.identifier.isiWOS:000299416100005-
dc.publisher.placeAustraliaen_US

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