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Article: Serum leptin and vascular risk factors in obstructive sleep apnea

TitleSerum leptin and vascular risk factors in obstructive sleep apnea
Authors
Issue Date2000
PublisherAmerican College of Chest Physicians. The Journal's web site is located at http://www.chestjournal.org
Citation
Chest, 2000, v. 118 n. 3, p. 580-586 How to Cite?
AbstractStudy objectives: To define the metabolic profile relevant to vascular risks in obstructive sleep apnea (OSA) and the role of leptin resistance in this risk profile. Design: Case control study. Setting: Sleep Laboratory, Queen Mary Hospital, University of Hong Kong, China. Methods: Thirty OSA subjects were matched with 30 non-OSA subjects for body mass index (BMI), age, sex, and menopausal status. Neck, waist, and hip girth, skinfold thickness, and fasting serum levels of lipids, glucose, insulin, and leptin were compared between these two groups. Results: Compared with control subjects with a similar BMI but without OSA, the OSA group had a significantly more adverse vascular risk factor profile, including dyslipidemia, higher diastolic BP, insulin resistance, and greater adiposity reflected by skinfold thickness. OSA subjects also had higher circulating leptin levels (9.18 ± 4.24 ng/mL vs 6.54 ± 3.81 ng/mL, mean ± SD, p = 0.001). Serum leptin levels correlated positively with BMI, skinfold thickness, serum cholesterol, low-density lipoprotein cholesterol, insulin, insulin/glucose ratio, apnea-hypopnea index, and oxygen desaturation time; multiple stepwise regression analysis identified skinfold thickness, waist/hip ratio, serum low-density lipoprotein cholesterol, and diastolic BP as independent correlates, while only serum insulin and diastolic BP were independent correlates in OSA subjects. After treatment with nasal continuous positive airway pressure for 6 months, there was a significant decrease in circulating leptin (p = 0.01) and triglyceride levels (p = 0.02) without change in other parameters. Conclusion: Despite controlling for BMI, OSA subjects showed distinct profiles with clustering of vascular risk factors. Hyperleptinemia was present in the OSA subjects, but it can be normalized by treatment with nasal continuous positive airway pressure, suggesting that increased leptin resistance was not the cause of OSA or its associated vascular risks.
Persistent Identifierhttp://hdl.handle.net/10722/77686
ISSN
2015 Impact Factor: 5.94
2015 SCImago Journal Rankings: 3.176
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorIp, MSMen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorHo, CMen_HK
dc.contributor.authorTsang, KWTen_HK
dc.contributor.authorLam, Wen_HK
dc.date.accessioned2010-09-06T07:34:37Z-
dc.date.available2010-09-06T07:34:37Z-
dc.date.issued2000en_HK
dc.identifier.citationChest, 2000, v. 118 n. 3, p. 580-586en_HK
dc.identifier.issn0012-3692en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77686-
dc.description.abstractStudy objectives: To define the metabolic profile relevant to vascular risks in obstructive sleep apnea (OSA) and the role of leptin resistance in this risk profile. Design: Case control study. Setting: Sleep Laboratory, Queen Mary Hospital, University of Hong Kong, China. Methods: Thirty OSA subjects were matched with 30 non-OSA subjects for body mass index (BMI), age, sex, and menopausal status. Neck, waist, and hip girth, skinfold thickness, and fasting serum levels of lipids, glucose, insulin, and leptin were compared between these two groups. Results: Compared with control subjects with a similar BMI but without OSA, the OSA group had a significantly more adverse vascular risk factor profile, including dyslipidemia, higher diastolic BP, insulin resistance, and greater adiposity reflected by skinfold thickness. OSA subjects also had higher circulating leptin levels (9.18 ± 4.24 ng/mL vs 6.54 ± 3.81 ng/mL, mean ± SD, p = 0.001). Serum leptin levels correlated positively with BMI, skinfold thickness, serum cholesterol, low-density lipoprotein cholesterol, insulin, insulin/glucose ratio, apnea-hypopnea index, and oxygen desaturation time; multiple stepwise regression analysis identified skinfold thickness, waist/hip ratio, serum low-density lipoprotein cholesterol, and diastolic BP as independent correlates, while only serum insulin and diastolic BP were independent correlates in OSA subjects. After treatment with nasal continuous positive airway pressure for 6 months, there was a significant decrease in circulating leptin (p = 0.01) and triglyceride levels (p = 0.02) without change in other parameters. Conclusion: Despite controlling for BMI, OSA subjects showed distinct profiles with clustering of vascular risk factors. Hyperleptinemia was present in the OSA subjects, but it can be normalized by treatment with nasal continuous positive airway pressure, suggesting that increased leptin resistance was not the cause of OSA or its associated vascular risks.en_HK
dc.languageengen_HK
dc.publisherAmerican College of Chest Physicians. The Journal's web site is located at http://www.chestjournal.orgen_HK
dc.relation.ispartofChesten_HK
dc.subject.meshAdulten_HK
dc.subject.meshBiological Markers - blooden_HK
dc.subject.meshBody Mass Indexen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeptin - blooden_HK
dc.subject.meshMaleen_HK
dc.subject.meshPositive-Pressure Respirationen_HK
dc.subject.meshRadioimmunoassayen_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshSleep Apnea, Obstructive - blood - complications - therapyen_HK
dc.subject.meshVascular Diseases - blood - etiology - prevention & controlen_HK
dc.titleSerum leptin and vascular risk factors in obstructive sleep apneaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0012-3692&volume=118&spage=582&epage=586&date=2000&atitle=Serum+leptin+and+vascular+risk+factors+in+obstructive+sleep+apneaen_HK
dc.identifier.emailIp, MSM:msmip@hku.hken_HK
dc.identifier.emailLam, KSL:ksllam@hku.hken_HK
dc.identifier.authorityIp, MSM=rp00347en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10988175-
dc.identifier.scopuseid_2-s2.0-0033801432en_HK
dc.identifier.hkuros57768en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033801432&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume118en_HK
dc.identifier.issue3en_HK
dc.identifier.spage580en_HK
dc.identifier.epage586en_HK
dc.identifier.isiWOS:000089383800007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridIp, MSM=7102423259en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridHo, CM=7404652540en_HK
dc.identifier.scopusauthoridTsang, KWT=7201555024en_HK
dc.identifier.scopusauthoridLam, W=7203021937en_HK

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