The role of obesity, different fat compartments and sleep apnea severity in circulating leptin levels: the Icelandic Sleep Apnea Cohort study
Objectives: To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level. Methods:...
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Published in | International Journal of Obesity Vol. 37; no. 6; pp. 835 - 842 |
---|---|
Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.06.2013
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 0307-0565 1476-5497 1476-5497 |
DOI | 10.1038/ijo.2012.138 |
Cover
Abstract | Objectives:
To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level.
Methods:
Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3±10.6 (mean±s.d.), body mass index (BMI) 32.7±5.3 kg m
−2
and apnea-hypopnea index 40.2±16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured.
Results:
Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume
per se
. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30–35 and BMI ⩾35 kg m
−2
). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (
P
=0.04). In
post-hoc
analysis for nonhypertensive OSA subjects (
n
=249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (
n
=199).
Conclusion:
Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects. |
---|---|
AbstractList | OBJECTIVES: To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level. METHODS: Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3 ± 10.6 (mean ± s.d.), body mass index (BMI) 32.7 ± 5.3 kg [m.sup.-2] and apnea-hypopnea index 40.2 ± 16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured. RESULTS: Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30-35 and BMI [greater than or equal to] 35kg [m.sup.-2]). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (P = 0.04). In post-hoc analysis for nonhypertensive OSA subjects (n = 249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (n = 199). CONCLUSION: Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects. International Journal of Obesity (2013) 37, 835-842; doi: 10.1038/ijo.2012.138; published online 11 September 2012 Keywords: obstructive sleep apnea; leptin; adipokine; visceral fat; subcutaneous fat; hypertension International Journal of Obesity (2013) 37, 835-842; doi: 10.1038/ijo.2012.138; published online 11 September 2012 To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level. Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3±10.6 (mean±s.d.), body mass index (BMI) 32.7±5.3kgm(-2) and apnea-hypopnea index 40.2±16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured. Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30-35 and BMI > or =35kgm(-2)). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (P=0.04). In post-hoc analysis for nonhypertensive OSA subjects (n=249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (n=199). Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects. To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level.OBJECTIVESTo assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level.Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3±10.6 (mean±s.d.), body mass index (BMI) 32.7±5.3 kg m(-2) and apnea-hypopnea index 40.2±16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured.METHODSCross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3±10.6 (mean±s.d.), body mass index (BMI) 32.7±5.3 kg m(-2) and apnea-hypopnea index 40.2±16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured.Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30-35 and BMI > or =35 kg m(-2)). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (P=0.04). In post-hoc analysis for nonhypertensive OSA subjects (n=249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (n=199).RESULTSLeptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30-35 and BMI > or =35 kg m(-2)). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (P=0.04). In post-hoc analysis for nonhypertensive OSA subjects (n=249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (n=199).Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects.CONCLUSIONObesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects. To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level. Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3±10.6 (mean±s.d.), body mass index (BMI) 32.7±5.3 kg m(-2) and apnea-hypopnea index 40.2±16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured. Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30-35 and BMI > or =35 kg m(-2)). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (P=0.04). In post-hoc analysis for nonhypertensive OSA subjects (n=249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (n=199). Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects. Objectives: To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level. Methods: Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3 plus or minus 10.6 (mean plus or minus s.d.), body mass index (BMI) 32.7 plus or minus 5.3 kg m super(-2) and apnea-hypopnea index 40.2 plus or minus 16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured. Results: Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se. No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30-35 and BMI greater than or equal to 35 kg m super(-2)). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity (P=0.04). In post-hoc analysis for nonhypertensive OSA subjects (n=249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects (n=199). Conclusion: Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects. Objectives: To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and whether the relationship between obstructive sleep apnea (OSA) severity and leptin levels differs depending on obesity level. Methods: Cross-sectional study of 452 untreated OSA patients (377 males and 75 females), in the Icelandic Sleep Apnea Cohort (ISAC), age 54.3±10.6 (mean±s.d.), body mass index (BMI) 32.7±5.3 kg m −2 and apnea-hypopnea index 40.2±16.1 events per h. A sleep study and magnetic resonance imaging of abdominal visceral and subcutaneous fat volume were performed, as well as fasting serum morning leptin levels were measured. Results: Leptin levels were more highly correlated with BMI, total abdominal and subcutaneous fat volume than visceral fat volume per se . No relationship was found between sleep apnea severity and leptin levels, assessed within three BMI groups (BMI <30, BMI 30–35 and BMI ⩾35 kg m −2 ). In a multiple linear regression model, adjusted for gender, BMI explained 38.7% of the variance in leptin levels, gender explained 21.2% but OSA severity did not have a significant role and no interaction was found between OSA severity and BMI on leptin levels. However, hypertension had a significant effect on the interaction between OSA severity and obesity ( P =0.04). In post-hoc analysis for nonhypertensive OSA subjects ( n =249), the association between leptin levels and OSA severity explained a minor but significant variance (3.2%) in leptin levels. This relationship was greatest for nonobese nonhypertensive subjects (significant interaction with obesity level). No relationship of OSA severity and leptin levels was found for hypertensive subjects ( n =199). Conclusion: Obesity and gender are the dominant determinants of leptin levels. OSA severity is not related to leptin levels except to a minor degree in nonhypertensive nonobese OSA subjects. |
Audience | Academic |
Author | Schwab, R J Maislin, G Benediktsdottir, B Pack, A I Jackson, N Arnardottir, E S Gislason, T Teff, K Juliusson, S |
AuthorAffiliation | 4 Monell Chemical Senses Center, Philadelphia, PA 6 Department of Otolaryngology, Landspitali - The National University Hospital of Iceland, Reykjavik, Iceland 5 Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA 2 Faculty of Medicine, University of Iceland 1 Dept of Respiratory Medicine and Sleep, Landspitali –The National University Hospital of Iceland, Reykjavik, Iceland 3 Center for Sleep and Circadian Neurobiology, Division of Sleep Medicine/Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA |
AuthorAffiliation_xml | – name: 6 Department of Otolaryngology, Landspitali - The National University Hospital of Iceland, Reykjavik, Iceland – name: 4 Monell Chemical Senses Center, Philadelphia, PA – name: 2 Faculty of Medicine, University of Iceland – name: 3 Center for Sleep and Circadian Neurobiology, Division of Sleep Medicine/Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA – name: 5 Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA – name: 1 Dept of Respiratory Medicine and Sleep, Landspitali –The National University Hospital of Iceland, Reykjavik, Iceland |
Author_xml | – sequence: 1 givenname: E S surname: Arnardottir fullname: Arnardottir, E S email: ernasif@landspitali.is organization: Department of Respiratory Medicine and Sleep, Landspitali—The National University Hospital of Iceland, Faculty of Medicine, University of Iceland, Division of Sleep Medicine/Department of Medicine, Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine – sequence: 2 givenname: G surname: Maislin fullname: Maislin, G organization: Division of Sleep Medicine/Department of Medicine, Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine – sequence: 3 givenname: N surname: Jackson fullname: Jackson, N organization: Division of Sleep Medicine/Department of Medicine, Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine – sequence: 4 givenname: R J surname: Schwab fullname: Schwab, R J organization: Division of Sleep Medicine/Department of Medicine, Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine – sequence: 5 givenname: B surname: Benediktsdottir fullname: Benediktsdottir, B organization: Department of Respiratory Medicine and Sleep, Landspitali—The National University Hospital of Iceland, Faculty of Medicine, University of Iceland – sequence: 6 givenname: K surname: Teff fullname: Teff, K organization: Monell Chemical Senses Center, Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania – sequence: 7 givenname: S surname: Juliusson fullname: Juliusson, S organization: Department of Otolaryngology, Landspitali—The National University Hospital of Iceland – sequence: 8 givenname: A I surname: Pack fullname: Pack, A I organization: Faculty of Medicine, University of Iceland, Division of Sleep Medicine/Department of Medicine, Center for Sleep and Circadian Neurobiology, University of Pennsylvania Perelman School of Medicine – sequence: 9 givenname: T surname: Gislason fullname: Gislason, T organization: Department of Respiratory Medicine and Sleep, Landspitali—The National University Hospital of Iceland, Faculty of Medicine, University of Iceland |
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ContentType | Journal Article |
Copyright | Macmillan Publishers Limited 2013 2014 INIST-CNRS COPYRIGHT 2013 Nature Publishing Group Copyright Nature Publishing Group Jun 2013 |
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Keywords | obstructive sleep apnea subcutaneous fat adipokine leptin visceral fat hypertension Visceral fat Hypertension Obesity Nervous system diseases Sleep apnea syndrome Adipose tissue Nutrition Respiratory disease Subcutaneous Nutrition disorder Cardiovascular disease Metabolic diseases Severity Adipokine Cohort study Leptin Fat Nutritional status Public health |
Language | English |
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PublicationTitle | International Journal of Obesity |
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To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of... To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of obesity and... OBJECTIVES: To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of... International Journal of Obesity (2013) 37, 835-842; doi: 10.1038/ijo.2012.138; published online 11 September 2012 Objectives: To assess whether sleep apnea severity has an independent relationship with leptin levels in blood after adjusting for different measures of... |
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Title | The role of obesity, different fat compartments and sleep apnea severity in circulating leptin levels: the Icelandic Sleep Apnea Cohort study |
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