{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T02:35:13Z","timestamp":1761964513676,"version":"3.37.3"},"reference-count":42,"publisher":"European Respiratory Society (ERS)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur Respir J"],"accepted":{"date-parts":[[2013,10,24]]},"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:p>There is increasing evidence that intermittent hypoxia resulting from obstructive sleep apnoea (OSA) is independently associated with dyslipidaemia. Currently, no data exist on potential links between OSA-related dyslipidaemia and susceptibility genes for dyslipidaemia in such patients. Our aim was to study the effects of the apolipoprotein E (<jats:italic>APOE<\/jats:italic>) genotype and sleep apnoea severity on atherogenic dyslipidaemia in patients with OSA.<\/jats:p><jats:p>519 clinically stable subjects prospectively recruited at a tertiary referral teaching hospital underwent full polysomnography.<jats:italic>APOE<\/jats:italic>gene polymorphisms were assessed using real-time PCR.<\/jats:p><jats:p>In all<jats:italic>APOE<\/jats:italic>genotype groups, serum triglycerides increased while high-density lipoprotein (HDL) cholesterol was reduced with increasing severity of OSA in each<jats:italic>APOE<\/jats:italic>genotype group, whereas the deleterious effects of OSA on serum apolipoprotein (Apo)B levels were observed in \u03f52 carriers and the \u03f53\/\u03f53 genotype only. Nevertheless, the \u03f54 allele carriers had ApoB levels within the risk range, irrespective of nocturnal hypoxia. In addition, among patients with the high-risk \u03f54 genotype, those with the most severe nocturnal hypoxia had significantly higher triglyceride and lower HDL cholesterol levels compared with nonhypoxic \u03f54 subjects.<jats:italic>APOE<\/jats:italic>genotype and the oxygen desaturation index were both independent predictors of serum triglyceride levels (p=0.009 and p&lt;0.001, respectively;<jats:italic>R<\/jats:italic><jats:sup>2<\/jats:sup>=0.148) and ApoB levels (p=0.001 and p=0.003, respectively;<jats:italic>R<\/jats:italic><jats:sup>2<\/jats:sup>=0.104).<\/jats:p><jats:p>Our findings suggest that OSA has adverse effects on several lipid parameters over and above the effects carried by<jats:italic>APOE<\/jats:italic>genotype. Further st1udies are needed to analyse the effects of high-risk genotypes on metabolic and cardiovascular outcomes in patients with OSA.<\/jats:p>","DOI":"10.1183\/09031936.00098513","type":"journal-article","created":{"date-parts":[[2013,11,15]],"date-time":"2013-11-15T02:43:27Z","timestamp":1384483407000},"page":"1097-1105","source":"Crossref","is-referenced-by-count":13,"title":["Effects of apolipoprotein E genotype on serum lipids in obstructive sleep 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