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Conference Paper: Metabolic associations of obstructive sleep apnoea

TitleMetabolic associations of obstructive sleep apnoea
Authors
Issue Date2008
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SBR
Citation
20th Annual Scientific Meeting of the Australasian Sleep Association and the 20th Annual Scientific Meeting of the Australasian Sleep Technologists Association, Adelaide, Australia, 2–4 October 2008. In Sleep and Biological Rhythms, 2008, v. 6 n. Supp 1, p. A7-A8 How to Cite?
AbstractIt has been observed in clinical practice and confirmed through epide-miologic and clinic-based studies that obstructive sleep apnoea (OSA) ishighly associated with various features of the metabolic syndrome,comprising of abdominal obesity, insulin resistance or glucose intoler-ance, dyslipidaemia, and hypertension. Most research has focused onthe association of OSA and various individual metabolic parameters,independent of obesity, the most common metabolic confounder inthese subjects. Studies have reported that OSA and periodic breathingare commonly seen in type 2 diabetic subjects. There is also increasingdata to support an adverse causal effect of OSA on insulin sensitivity/resistance in both adults and children, although rigorous evidence frominterventional studies are still needed to show that treating OSA can leadto improved insulin sensitivity/resistance in non-diabetics or better gly-cemic control in diabetics. Another metabolic disorder, dyslipidaemia,is also commonly seen in subjects with OSA although the exact lipidparameter that has reported to be deranged vary from total cholesterolto HDL-cholesterol to triglycerides. Data on an independent effect ofOSA on dyslipidaemia has not been consistent, and effect of CPAPtreatment have been mostly derived from observational studies. Thereare multiple pathophysiologic mechanisms in OSA which may poten-tially give rise to metabolic dysregulation, including intermittenthypoxia, sleep fragmentation and sympathetic activation, which may in turn affect the expression of intermediary mediators. Translationalstudies have also shown dysregulation of various inflammatory cytok-ines or adipokines which may potentially lead to adverse metaboliceffects. Animal experiments exposed to intermittent hypoxia, as a modelof OSA, have shown deleterious effects on glucose and lipid regulation.However, results of these studies are not always consistent and causalityof OSA on metabolic dysfunction remains a controversial issue. Mean-while, healthcare professionals should be aware of the high associationand encouraged to look for metabolic derangements in subjects withOSA and vice versa, and treatment given to each disorder as appropriate.
Persistent Identifierhttp://hdl.handle.net/10722/62443
ISSN
2015 Impact Factor: 0.628
2015 SCImago Journal Rankings: 0.293

 

DC FieldValueLanguage
dc.contributor.authorIp, MSM-
dc.date.accessioned2010-07-13T04:01:20Z-
dc.date.available2010-07-13T04:01:20Z-
dc.date.issued2008-
dc.identifier.citation20th Annual Scientific Meeting of the Australasian Sleep Association and the 20th Annual Scientific Meeting of the Australasian Sleep Technologists Association, Adelaide, Australia, 2–4 October 2008. In Sleep and Biological Rhythms, 2008, v. 6 n. Supp 1, p. A7-A8-
dc.identifier.issn1446-9235-
dc.identifier.urihttp://hdl.handle.net/10722/62443-
dc.description.abstractIt has been observed in clinical practice and confirmed through epide-miologic and clinic-based studies that obstructive sleep apnoea (OSA) ishighly associated with various features of the metabolic syndrome,comprising of abdominal obesity, insulin resistance or glucose intoler-ance, dyslipidaemia, and hypertension. Most research has focused onthe association of OSA and various individual metabolic parameters,independent of obesity, the most common metabolic confounder inthese subjects. Studies have reported that OSA and periodic breathingare commonly seen in type 2 diabetic subjects. There is also increasingdata to support an adverse causal effect of OSA on insulin sensitivity/resistance in both adults and children, although rigorous evidence frominterventional studies are still needed to show that treating OSA can leadto improved insulin sensitivity/resistance in non-diabetics or better gly-cemic control in diabetics. Another metabolic disorder, dyslipidaemia,is also commonly seen in subjects with OSA although the exact lipidparameter that has reported to be deranged vary from total cholesterolto HDL-cholesterol to triglycerides. Data on an independent effect ofOSA on dyslipidaemia has not been consistent, and effect of CPAPtreatment have been mostly derived from observational studies. Thereare multiple pathophysiologic mechanisms in OSA which may poten-tially give rise to metabolic dysregulation, including intermittenthypoxia, sleep fragmentation and sympathetic activation, which may in turn affect the expression of intermediary mediators. Translationalstudies have also shown dysregulation of various inflammatory cytok-ines or adipokines which may potentially lead to adverse metaboliceffects. Animal experiments exposed to intermittent hypoxia, as a modelof OSA, have shown deleterious effects on glucose and lipid regulation.However, results of these studies are not always consistent and causalityof OSA on metabolic dysfunction remains a controversial issue. Mean-while, healthcare professionals should be aware of the high associationand encouraged to look for metabolic derangements in subjects withOSA and vice versa, and treatment given to each disorder as appropriate.-
dc.languageeng-
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SBR-
dc.relation.ispartofSleep and Biological Rhythms-
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.titleMetabolic associations of obstructive sleep apnoea-
dc.typeConference_Paper-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.authorityIp, MSM=rp00347-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1479-8425.2008.00359_1.x-
dc.identifier.hkuros162732-
dc.identifier.volume6-
dc.identifier.issueSupp 1-
dc.identifier.spageA7-
dc.identifier.epageA8-
dc.publisher.placeAustralia-

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