The Effect of Acute Intermittent Hypoxia on Postprandial Lipid Metabolism

FieldValue
dc.contributor.authorMorin, Renée
dc.date.accessioned2020-05-22T19:26:41Z
dc.date.available2020-05-22T19:26:41Z
dc.date.issued2020-05-22
dc.identifier.urihttp://hdl.handle.net/10393/40537
dc.identifier.urihttp://dx.doi.org/10.20381/ruor-24768
dc.description.abstractBackground: Obstructive sleep apnea (OSA) consists of repeated, involuntary breathing suspension during sleep. These events induce rapid depletion/repletion of blood/tissue oxygen content, a phenomenon known as intermittent hypoxia. Aside from causing daytime sleepiness, the most important health consequence of OSA is a 2-fold increase in cardiovascular (CVD) risk. Animal studies provide evidence that intermittent hypoxia, a simulating model of OSA, causes important rise in plasma TG, especially in the postprandial state. However, the underpinning mechanisms linking intermittent hypoxia to altered postprandial TG levels remain unknown. As such, the objective of this study was to characterize the effects of acute intermittent hypoxia on postprandial TG levels in 2 distinct lipoprotein subtypes in humans: chylomicrons which are secreted by the intestine and carry dietary lipids, and denser TG carriers (mainly VLDL) which are secreted by the liver and carry endogenous lipids. Methods: The research consisted of a randomized crossover design. In collaboration with the Sleep laboratory at Montfort Hospital, 7 individuals diagnosed with moderate sleep apnea were recruited through phone calls as well as 8 healthy individuals without OSA from the University of Ottawa. While lying on a bed, participants were given a meal after which they were exposed for 6 hours to normoxia or intermittent hypoxia corresponding to moderate OSA, e.g. 15 hypoxic events per hour. Blood lipid levels were measured hourly.  Results: Plasma TG levels increased over time in both experimental conditions and tended to be greater under 6-h exposure to intermittent hypoxia (p=0.093, effect size ηp2= 0.383.). This trend toward higher total plasma TG under intermittent hypoxia was attributable to increased levels in denser TG carrying lipoproteins such as VLDL and CM remnants (p= 0.009, ηp2 = 0.173).  Conclusion: Acute intermittent hypoxia, a simulating model of obstructive sleep apnea, tends to negatively affect postprandial TG levels, which is attributable to an increase in denser TG carrying lipoprotein levels such as VLDL and CM remnants. These results lend support to the increase in blood lipid levels in animal studies observing the effect of acute hypoxia in mice.  Contribution to advancement of knowledge: This proposed research will allow a better understanding of the mechanisms by which obstructive sleep apnea may alter blood lipid profile. This information will be beneficial to the treatment of obstructive sleep apnea related dyslipidemia and contribute to reduce CVD risk in the large proportion of obstructive sleep apnea patients who are reluctant to current treatment avenues. 
dc.language.isoen
dc.publisherUniversité d'Ottawa / University of Ottawa
dc.subjectIntermittent hypoxia
dc.subjectTriglycerides
dc.subjectPostprandial
dc.subjectLipoproteins
dc.subjectObstructive sleep apnea
dc.titleThe Effect of Acute Intermittent Hypoxia on Postprandial Lipid Metabolism
dc.typeThesis
dc.contributor.supervisorImbeault, Pascal
thesis.degree.nameMSc
thesis.degree.levelMasters
thesis.degree.disciplineSciences de la santé / Health Sciences
uottawa.departmentSciences de l'activité physique / Human Kinetics
CollectionThèses, 2011 - // Theses, 2011 -

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