Serum leptin and vascular risk factors in obstructive sleep apnea

Citation
Msm. Ip et al., Serum leptin and vascular risk factors in obstructive sleep apnea, CHEST, 118(3), 2000, pp. 580-586
Citations number
41
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
00123692 → ACNP
Volume
118
Issue
3
Year of publication
2000
Pages
580 - 586
Database
ISI
SICI code
0012-3692(200009)118:3<580:SLAVRF>2.0.ZU;2-Y
Abstract
Study objectives: To define the metabolic profile relevant to vascular risk s in obstructive sleep apnea (OSA) and the role of leptin resistance in thi s risk profile. Design: Case control study. Setting: Sleep Laboratory, Queen Mary Hospital, University of Hong Kong, Ch ina. 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 gi rth, skinfold thickness, and fasting serum levels of lipids, glucose, insul in, 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 profil e, including dyslipidemia, higher diastolic BP, insulin resistance, and gre ater adiposity reflected by skinfold thickness, OSA subjects also had highe r circulating leptin levels (9.18 +/- 4.24 ng/mL vs 6.54 +/- 3.81 ng/mL, me an +/- 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 desaturat ion time; multiple stepwise regression analysis identified skinfold thickne ss, waist/hip ratio, serum low-density lipoprotein cholesterol, and diastol ic BP as independent correlates, while only serum insulin and diastolic BP were independent correlates in OSA subjects. After treatment with nasal con tinuous positive airway pressure for 6 months, there was a significant decr ease in circulating leptin (p = 0.01) and triglyceride levels (p = 0.02) wi thout change in other parameters. Conclusion: Despite controlling for BMI, OSA subjects showed distinct profi les with clustering of vascular risk factors. Hyperleptinemia was present i n the OSA subjects, but it can be normalized by treatment with nasal contin uous positive airway pressure, suggesting that increased leptin resistance was not the cause of OSA or its associated vascular risks.