M S Ip1, K S Lam, C Ho, K W Tsang, W Lam. 1. Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China. msmip@hkucc.hku.hk
Abstract
STUDY 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.
STUDY 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.
Authors: Ronghua Yang; Gautam Sikka; Jill Larson; Vabren L Watts; Xiaolin Niu; Carla L Ellis; Karen L Miller; Andre Camara; Christian Reinke; Vladimir Savransky; Vsevolod Y Polotsky; Christopher P O'Donnell; Dan E Berkowitz; Lili A Barouch Journal: Am J Physiol Heart Circ Physiol Date: 2011-01-28 Impact factor: 4.733
Authors: Patrícia Caetano Mota; Marta Drummond; João Carlos Winck; Ana Cristina Santos; João Almeida; José Agostinho Marques Journal: Sleep Breath Date: 2010-09-24 Impact factor: 2.816
Authors: Ioannis Papaioannou; Michael Patterson; Gillian L Twigg; Ali Vazir; Mohammad Ghatei; Mary J Morrell; Michael I Polkey Journal: J Clin Sleep Med Date: 2011-10-15 Impact factor: 4.062
Authors: Karen A Waters; Sinthu Sitha; Louise M O'brien; Sherryn Bibby; Carina de Torres; Silvano Vella; Roland de la Eva Journal: Am J Respir Crit Care Med Date: 2006-05-18 Impact factor: 21.405
Authors: Steven D Shapiro; Chien-Hung Chin; Jason P Kirkness; Brian M McGinley; Susheel P Patil; Vsevolod Y Polotsky; Paolo Jose Cesare Biselli; Philip L Smith; Hartmut Schneider; Alan R Schwartz Journal: J Appl Physiol (1985) Date: 2014-02-20