Annals of Thoracic Medicine Official publication of the Saudi Thoracic Society, affiliated to King Saud University
 
Search Ahead of print Current Issue Archives Instructions Subscribe e-Alerts Login 
Home Email this article link Print this article Bookmark this page Decrease font size Default font size Increase font size


 
ORIGINAL ARTICLE
Year : 2010  |  Volume : 5  |  Issue : 3  |  Page : 161-165
Ghrelin, leptin, adiponectin, and resistin levels in sleep apnea syndrome: Role of obesity


1 Department of Pulmonary Medicine, School of Medicine, University of Uludag, Bursa, Turkey
2 Department of Biochemistry, School of Medicine, University of Uludag, Bursa, Turkey

Date of Submission19-Dec-2009
Date of Acceptance18-May-2010
Date of Web Publication2-Jul-2010

Correspondence Address:
Ahmet Ursavas
Department of Pulmonary Medicine, School of Medicine, University of Uludag, Bursa
Turkey
Login to access the Email id


DOI: 10.4103/1817-1737.65050

PMID: 20835311

Get Permissions

   Abstract 

Aim: The aim of this study was to investigate the relationship among plasma leptin, ghrelin, adiponectin, resistin levels, and obstructive sleep apnea syndrome (OSAS).
Methods: Fifty-five consecutive newly diagnosed OSAS patients and 15 age-matched nonapneic controls were enrolled in this study. After sleep study between 8:00 AM and 9:00 AM on the morning, venous blood was obtained in the fasting state to measure ghrelin and adipokines.
Results: Serum ghrelin levels of OSAS group were significantly (P < 0.05) higher than those of the control group. No significant difference was noted in the levels of leptin, adiponectin, and resistin in OSAS group when compared to controls. There was a significant positive correlation between ghrelin and apnea-hypopnea index (AHI) (r = 0.237, P < 0.05) or the Epworth sleepiness scale (ESS) (r = 0.28, P < 0.05). There was also a significant positive correlation between leptin and body mass index (r = 0.592, P < 0.0001). No significant correlation was observed between leptin, adiponectin, resistin, and any polysomnographic parameters.
Conclusion : Our findings demonstrated that serum ghrelin levels were higher in OSAS patients than those of control group and correlated with AHI and ESS. Further studies are needed to clarify the complex relation among OSAS, obesity, adipokines, and ghrelin.


Keywords: Adipokines, obesity, sleep apnea


How to cite this article:
Ursavas A, Ilcol YO, Nalci N, Karadag M, Ege E. Ghrelin, leptin, adiponectin, and resistin levels in sleep apnea syndrome: Role of obesity. Ann Thorac Med 2010;5:161-5

How to cite this URL:
Ursavas A, Ilcol YO, Nalci N, Karadag M, Ege E. Ghrelin, leptin, adiponectin, and resistin levels in sleep apnea syndrome: Role of obesity. Ann Thorac Med [serial online] 2010 [cited 2014 Sep 18];5:161-5. Available from: http://www.thoracicmedicine.org/text.asp?2010/5/3/161/65050


Obstructive sleep apnea syndrome (OSAS) is characterized by repetitive collapse of the upper airway during sleep, resulting in impedance to airflow and oxygen desaturations, which cause arousal from sleep. [1] OSAS is strongly associated with obesity, approximately 70% of OSAS patients are obese and obesity is the only reversible risk factor of importance. [2],[3]

Leptin is a circulating hormone that is expressed abundantly throughout the body specifically in adipose tissue. The primary role of leptin is in controlling appetite. [4] Adiponectin is the adipokine that circulates at the highest. Resistin is a member of cysteine-rich secretory proteins. [5] Leptin and resistin have been shown to exert potent pro-inflammatory properties by upregulating pro-inflammatory cytokines. On the other hand, adiponectin reduces the production and activity inflammatory cytokine. [6] Ghrelin is a 28 amino acid peptide hormone, has an appetite-stimulating effect and controls the energy balance. [7]

OSAS is strongly associated with obesity and inflammation. With the growing prevalence of obesity, scientific interest in the biology of adipose tissue has been extended to the secretory products of adipocytes. Human obesity is associated with increased leptin, resistin levels, and decreased adiponectin levels. [8],[9],[10],[11] The plasma ghrelin level is lower in obese subjects than in nonobese subjects. [7] Several studies suggest that there are significant relationships among obesity, adipokines, systemic inflammation, and atherosclerosis. [12],[13]

Although association of obesity, leptin, ghrelin, and inflammations well documented, role of adipokines and ghrelin in OSAS remains controversial. The objectives of this study were twofold. First, we sought to determine and compare the levels of serum leptin, ghrelin, resistin, and adiponectin in OSAS patients and nonapneic controls. Second, we sought to determine relationship between adipokines each other and some sleep parameters. To the best of our knowledge, this is the first reported attempt to assess these adipokines and ghrelin in OSAS patients.


   Methods Top


Subjects

A cross-sectional study was performed, which included subjects referred to the same sleep center for the investigation for snoring or possible OSAS. Fifty-five consecutive newly diagnosed OSAS patients and 15 age-matched nonapneic controls were enrolled in this study. Subjects with heart failure, chronic renal failure, chronic obstructive pulmonary disease, on systemic steroid treatments, and on hormonal replacement therapy were excluded from the study.

All subjects were asked to complete a questionnaire about the presence of any history of snoring, witnessed apnea, excessive daytime sleepiness, Epworth Sleepiness Scale (ESS), medical history, and medication. Demographic information (age, gender, and smoking habits) and anthropometric measurements including height, weight, body mass index (BMI): weight/height (kg/m 2 ) were obtained on presentation to the sleep center.

The study protocol was approved by the Ethics Committee of the Uludag University Medical Hospital, Bursa, Turkey. All patients gave written informed consent to participate in this study.

Sleep analysis

Full polysomnography (PSG) monitoring was performed on all participants using the Compumedics P-series Sleep System (Compumedics Sleep: Melbourne, Australia). All participants reported to the sleep laboratory at approximately 8.30 PM, and PSG was initiated at approximately 8.30 PM. Polysomnographic recordings included two electro-encephalography (EEG) channels (C3/A2 and O2/A1), two electro-oculogram (EOG) channels, one submental electromyogram (EMG) channel, and one electrocardiography (ECG) channel. Ventilatory monitoring included recording of oronasal airflow (with an oronasal thermistor), hemoglobin oxygen saturation by pulse oximetry (SaO 2 was measured via a finger oximeter), respiratory movement (with an inductive plethysmography), including chest and abdomen, and body position.

Sleep staging was performed according to the standard criteria of Rechtschaffen and Kales. [14] To assess ventilation during sleep, nasal airflow was analyzed carefully. Apnea was defined as episodes of airflow cessation lasting ≥10 s. Hypopnea was defined as episodes lasting ≥10 s, with reductions of thermistor signal amplitude ≥50% and an associated fall of ≥3% in oxygen saturation, or an arousal that lasted ≥10 s. The sum of time spent in apnea and hypopnea was divided by the total sleep time to determine the apnea-hypopnea index (AHI). Subjects with AHI ≥ 5 were considered to have OSAS. Subjects with AHI < 5 were included in the control group.

Serum leptin, ghrelin, adiponectin, and resistin assays

After sleep study between 8:00 AM and 9:00 AM on the morning, venous blood was obtained in the fasting state to measure ghrelin and adipokines. Blood samples were centrifuged with in 30 min at 4°C for at 3000 Χ g for 10 min. Serum samples were stored at -80°C until performance of assay.

Serum adiponectin, leptin, and ghrelin levels were measured by radioimmunoassay using a commercially available kit (Linco Research, St. Charles, MO, USA). All serum samples from individual subjects were assayed in duplicate in the same test battery. Within and between assay coefficients of variations were <6% and <7%, <5% and <8%, or <7% and <10% for adiponectin, leptin, or ghrelin, respectively. The lowest level of human leptin and ghrelin that can be detected by the assay kits was 0.5 ng/mL and 95 pg/mL when using a 100 μL undiluted serum sample, respectively. For serum adiponectin measurement, serum samples were diluted by 1/500 with assay buffer as advised. The lowest level of human adiponectin that can be detected by the assay was 1 ng/mL when using a 100 μL of diluted (1/500) serum sample.

Serum resistin levels were measured using a commercially available ELISA kit (Linco Research, St. Charles, MO, USA). All serum samples from individual subjects were assayed in duplicate in the same test battery. Within and between assay coefficients of variations were <5% and <7%, respectively. The lowest level of human resistin that can be detected by this assay was 0.16 ng/mL.

Statistical analysis

Statistical analysis was performed using the SPSS package for Windows, version 13.0 (SPSS, Inc., Chicago, IL, USA). Comparisons between data of the OSAS and control groups were carried out with Student's t-test, Chi-square test, and the Mann-Whitney U-test. The concordance of normal distribution of all variables was calculated with the Shapiro-Wilk test before comparison between OSAS and control groups. If the data were not normally distributed, we used nonparametric tests for dependant variables. Relationship between serum adipokines levels and ESS, number of total apnea, number of total respiratory events, time spent in apnea and hypopnea, average oxygen desaturation, oxygen desaturation index, REM sleep, slow wave sleep, and respiratory arousal index were calculated using the Pearson correlation analysis. P value <0.05 was considered statistically significant.


   Results Top


Baseline characteristics

Baseline characteristic of the study population are shown in [Table 1]. There were 10 diabetic and 15 hypertensive patients in OSAS group. There was no significant difference in age, gender, BMI, smoking habit, and snoring between the two groups. In the OSAS group, excessive daytime sleepiness and ESS scores were significantly higher than those of the control group (P < 0.001). There were no significant differences in the total sleeping time, sleep efficiency, and baseline oxygen saturation between the two groups. Significant differences (P < 0.05-0.001) in sleep Stages 3 and 4, arousal (per hour), AHI, duration of apnea-hypopnea, oxygen desaturation index, average oxygen saturation during sleep, average oxygen desaturation, and length of time spent with an oxygen saturation <90% were noted when the OSAS group was compared to control group [Table 1].

Serum leptin, grelin, adiponectin, and resistin levels

Serum levels of leptin, ghrelin, adiponectin, and resistin of the two groups are shown in [Table 2]. The serum levels of ghrelin in the OSAS group (564 ± 44 pg/mL) were significantly (P < 0.05) higher than those of the control group (403 ± 90 pg/mL). No significant difference was noted in the levels of leptin, adiponectin, and resistin in OSAS group when compared to controls.

There was a significant positive correlation between ghrelin and AHI [Figure 1] or ESS (r = 0.28, P < 0.05) [Figure 2], and negative correlation was also noted between ghrelin and resistin (r = -0.39, P < 0.05). There was a significant positive correlation between leptin and BMI (r = 0.59, P < 0.0001) [Figure 3]. There was no significant correlation between adipokines and any polysomnographic parameters.


   Discussion Top


The results of our study indicated that the serum levels of ghrelin in the OSAS group were significantly higher than those of the nonapneic control group. There was a significant positive correlation among serum levels of ghrelin, AHI, and ESS. No significant difference was noted in the levels of leptin, adiponectin, and resistin in OSAS group compared to controls. There was a significant positive correlation between leptin and BMI.

Serum level of leptin is correlated with BMI in humans. [15] Leptin levels were found increased in patients with OSAS. However, several studies suggested that these abnormal leptin levels may be related to the obesity, sympathetic activity, and hypoxia in patients with OSAS. [16],[17],[18] Tatsumi et al.[17] indicated that circulating leptin levels were correlated with body mass index (BMI), visceral fat accumulation (VFA), subcutaneous fat accumulation (SFA), apnea-hypopnea index (AHI), sleep mean arterial oxygen saturation, and sleep lowest arterial oxygen saturation. Multiple regression analysis revealed that average oxygen saturation and lowest oxygen saturation were explanatory variables for serum leptin values, but AHI (P = 0.054), BMI, VFA, and SFA were not. It was suggested that sleep hypoxemia may be the main determinant of circulating leptin levels. Shimura et al.[18] demonstrated that circulating leptin levels correlated with BMI, VFA, and SFA, but not with PaO 2 or sleep mean arterial oxygen saturation. They reported that leptin levels were higher in the hypercapnic group than in the eucapnic group. Serum leptin was the only predictor for the presence of hypercapnia in logistic regression analysis. Shimizu et al.[19] reported that plasma leptin reached a peak level at 00:00 hours in patients with OSAS, both with and without continuous positive airway pressure (CPAP) treatment. The magnitude of the decrease in leptin levels after CPAP treatment was significantly correlated with cardiac sympathetic function measured before CPAP treatment. They suggested that serum leptin levels in the morning may be a marker of improved cardiac sympathetic nerve function.

On the other hand, Barcelo et al.[20] compared the levels of leptin in four groups, obese and nonobese with OSAS compared with obese and nonobese controls. They did not find any significant difference in the leptin levels between the groups. In recent study, Sharma et al.[21] reported that no significant difference was noted in levels of fasting blood sugar, insulin resistance, leptin, or adiponectin in OSAS group compared the obese controls. In this study, we showed that no significant difference was noted in the levels of leptin in OSAS group when compared to controls, there was not significant correlation among AHI, mean oxygen saturation in sleep, mean oxygen desaturation in sleep, oxygen desaturation index, and serum leptin levels. We only found a significant positive correlation between leptin levels and BMI.

Adiponectin has the biological effects of anti-inflammatory, anti-atherosclerosis, increasing insulin sensitivity and decreasing insulin resistance. [22] It has been reported that there is a significant relationship between OSAS and decreased serum level of adiponectin; [23] however, other studies found a normal or increased adiponectin level in patients with OSAS. [21],[24],[25] Zhang et al.[23] reported that serum adiponectin levels were significantly lower in the OSAS group than in the control. Makino et al.[24] examined that 213 patients with OSAS were divided into three groups: 30 with mild, 98 moderate, and 85 with severe OSAS. They determined plasma adiponectin levels were not different among mild, moderate, and severe OSAS groups. They suggested that plasma adiponectin was more closely related to obesity than to sleep apnea. Tauman et al.[25] indicated that adiponectin levels were lower in obese than nonobese children and were inversely correlated with BMI Z scores but not with AHI. In this study, we showed that no significant difference was noted in the levels of adiponectin in OSAS group compared to controls.

Resistin is new white adipose tissue hormone. Its linkage to obesity and OSAS were controversial in previous studies. [25],[26],[27],[28] Harsch et al.[27] reported that while resistin levels were positively correlated with IL-6, CRP, ICAM-1, and leptin, negatively correlated with insulin sensitivity index. No correlation was observed between BMI or AHI and resistin levels. They found that resistin remained unchanged during CPAP therapy. In the recent study, adiponectin and resistin levels were compared with in simple obesity, obese OSAS patients, and multiple symmetrical lipomatosis (LBS), and they found no significant differences in serum adiponectin and resistin levels between these groups. [28] In this study, we showed that no significant difference was noted in the levels of resistin in OSAS group compared to controls.

Serum ghrelin levels are inversely related to changes of body weight. It is highest in anorectic subjects and low in obese persons. [29] Relationship between serum ghrelin level and OSAS is controversial. It has been suggested that reduced total sleep time can lead to alterations in parameters of glucose tolerance and dysregulation of appetite. [30] OSAS also involves respiratory stress in addition to sleep loss and sleep fragmentation, and hypoxia and hypercapnia also result in increases in sympathetic nerve activity. Ghrelin release may be related to sympathetic activation in OSAS. Harsch et al.[31] showed that baseline plasma ghrelin levels were significantly higher in OSAS patients than in controls. After 2 days of CPAP treatment, plasma ghrelin decreased in almost all OSAS patients to levels that were only slightly higher than those of controls. Ulukavak et al.[32] investigated serum leptin and ghrelin levels in obese patients with OSAS in comparison with equally obese controls without OSAS. They indicated that significantly higher serum leptin levels were found in OSAS patients compared to controls, but there was no significant difference in serum ghrelin levels between OSAS patients and controls. In this study, we showed that the circulating levels of ghrelin in the OSAS group were significantly higher than those of the control group and there was a significant positive correlation between ghrelin and AHI.

Potential limitations of this study merit consideration. First, we used oronasal thermistor for measured oronasal air flow. Second, this is a cross-sectional study and our sample size is limited. Finally, our control group subjects were not healthy people from population.

In conclusion, we found no relationship between adipokines and OSAS. On the contrary, serum levels of ghrelin was higher in OSAS patients. We suggest that there are several confounding factors such as obesity, repetitive hypoxia, hypercapnia, and sympathetic activation which can be influence serum adipokines and ghrelin levels in patients with OSAS. These factors may be reason of inconsistent results in several studies.

 
   References Top

1.ASDA-Diagnostic Classification Steering Committee. The international classification of sleep disorders. Diagnostic and Coding Manual. 2nd ed. Lawrance, KS: Allen Press Inc; 1997.  Back to cited text no. 1      
2.Strollo PJ Jr, Rogers RM. Obstructive sleep apnea. N Engl J Med 1996;334:99-104.  Back to cited text no. 2      
3.Malhotra A, White DP. Obstructive sleep apnoea. Lancet 2002;360:237-45.  Back to cited text no. 3      
4.Alam I, Lewis K, Stephens JW, Baxter JN. Obesity, metabolic syndrome and sleep apnoea: All pro-inflammatory states. Obes Rev 2007;8:119-27.  Back to cited text no. 4      
5.Auwerx J, Staels B. Leptin. Lancet 1998;351:737-42.  Back to cited text no. 5      
6.Masaki T, Chiba S, Tatsukawa H, Yasuda T, Noguchi H, Seike M, et al. Adiponectin protects LPS-induced liver injury through modulation of TNF-alpha in KK-Ay obese mice. Hepatology 2004;40:177-84.  Back to cited text no. 6      
7.Cummings DE, Purnell JQ, Frayo RS, Schmidova K, Wisse BE, Weigle DS. A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes 2001;50:1714-9.  Back to cited text no. 7      
8.Lebovitz HE. The relationship of obesity to the metabolic syndrome. Int J Clin Pract Suppl 2003;134:18-27.  Back to cited text no. 8      
9.Ronti T, Lupattelli G, Mannarino E. The endocrine function of adipose tissue: An update. Clin Endocrinol (Oxf) 2006;64:355-65.  Back to cited text no. 9      
10.O'Donnell CP, Tankersley CG, Polotsky VP, Schwartz AR, Smith PL. Leptin, obesity, and respiratory function. Respir Physiol 2000;119:163-70.  Back to cited text no. 10      
11.Chandran M, Phillips SA, Ciaraldi T, Henry RR. Adiponectin: More than just another fat cell hormone? Diabetes Care 2003;26:2442-50.  Back to cited text no. 11      
12.Sφderberg S, Ahrιn B, Jansson JH, Johnson O, Hallmans G, Asplund K, et al. Leptin is associated with increased risk of myocardial infarction. J Intern Med 1999;246:409-18.  Back to cited text no. 12      
13.Aizawa-Abe M, Ogawa Y, Masuzaki H, Ebihara K, Satoh N, Iwai H, et al. Pathophysiological role of leptin in obesity-related hypertension. J Clin Invest 2000;105:1243-52.  Back to cited text no. 13      
14.Allan Rechtschaffen In: Rechtschaffen A, Kales A, editors. A manual of standardized terminology, tecniques and scoring system for sleep stages of human subjects. 3rd ed. Los Angeles: Brain Research Institute; 1973. p. 1-13.  Back to cited text no. 14      
15.Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, et al. Serum immunreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med 1996;334:292-5.  Back to cited text no. 15      
16.Ip MS, Lam KS, Ho C, Tsang KW, Lam W. Serum leptin and vascular risk factors in obstructive sleep apnea. Chest 2000;118:580-6.  Back to cited text no. 16      
17.Tatsumi K, Kasahara Y, Kurosu K, Tanabe N, Takiguchi Y, Kuriyama T. Sleep oxygen desaturation and circulating leptin in obstructive sleep apnea-hypopnea syndrome. Chest 2005;127:716-21.  Back to cited text no. 17      
18.Shimura R, Tatsumi K, Nakamura A, Kasahara Y, Tanabe N, Takiguchi Y, et al. Fat accumulation, leptin, and hypercapnia in obstructive sleep apnea-hypopnea syndrome. Chest 2005;127:543-9.  Back to cited text no. 18      
19.Shimizu K, Chin K, Nakamura T, Masuzaki H, Ogawa Y, Hosokawa R, et al. Plasma leptin levels and cardiac sympathetic function in patients with obstructive sleep apnoea-hypopnoea syndrome. Thorax 2002;57:429-34.  Back to cited text no. 19      
20.Barcelσ A, Barbι F, Llompart E, de la Peρa M, Durαn-Cantolla J, Ladaria A, et al. Neuropeptide Y and leptin in patients with obstructive sleep apnea syndrome: Role of obesity. Am J Respir Crit Care Med 2005;171:183-7.  Back to cited text no. 20      
21.Sharma SK, Kumpawat S, Goel A, Banga A, Ramakrishnan L, Chaturvedi P. Obesity, and not obstructive sleep apnea, is responsible for metabolic abnormalities in a cohort with sleep-disordered breathing. Sleep Med 2007;8:12-7.  Back to cited text no. 21      
22.Wulster-Radcliffe MC, Ajuwon KM, Wang J, Christian JA, Spurlock ME. Adiponectin differntially regulates cytokines in porcine macrophages. Biochem Biophys Res Commun 2004;316:924-9.  Back to cited text no. 22      
23.Zhang XL, Yin KS, Wang H, Su S. Serum adiponectin levels in adult male patients with obstructive sleep apnea hypopnea syndrome. Respiration 2006;73:73-7.  Back to cited text no. 23      
24.Makino S, Handa H, Suzukawa K, Fujiwara M, Nakamura M, Muraoka S, et al. Obstructive sleep apnoea syndrome, plasma adiponectin levels, and insulin resistance. Clin Endocrinol (Oxf) 2006;64:12-9.  Back to cited text no. 24      
25.Tauman R, Serpero LD, Capdevila OS, O'Brien LM, Goldbart AD, Kheirandish-Gozal L, et al. Adipokines in children with sleep disordered breathing. Sleep 2007;30:443-9.  Back to cited text no. 25      
26.Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, et al. The hormone resistin links obesity to diabetes. Nature 2001;409:307-12.  Back to cited text no. 26      
27.Harsch IA, Koebnick C, Wallaschofski H, Schahin SP, Hahn EG, Ficker JH, et al. Resistin levels in patients with obstructive sleep apnoea syndrome--the link to subclinical inflammation? Med Sci Monit 2004;10:CR510-5.  Back to cited text no. 27      
28.Harsch IA, Bergmann T, Koebnick C, Wiedmann R, Ruderich F, Hahn EG, et al. Adiponectin, resistin and subclinical inflammation--the metabolic burden in Launois Bensaude syndrome, a rare form of obesity. J Physiol Pharmacol 2007;58:65-76.  Back to cited text no. 28      
29.Tschφp M, Weyer C, Tataranni PA, Devanarayan V, Ravussin E, Heiman ML. Circulating ghrelin levels are decreased in human obesity. Diabetes 2001;50:707-9.  Back to cited text no. 29      
30.Spiegel K, Knutson K, Leproult R, Tasali E, Van Cauter E. Sleep loss: A novel risk factor for insulin resistance and type 2 diabetes. J Appl Physiol 2005;99:2008-19.   Back to cited text no. 30      
31.Harsch IA, Konturek PC, Koebnick C, Kuehnlein PP, Fuchs FS, Pour Schahin S, et al. Leptin and ghrelin levels in patients with obstructive sleep apnoea: Effect of CPAP treatment. Eur Respir J 2003;22:251-7.  Back to cited text no. 31      
32.Ulukavak Ciftci T, Kokturk O, Bukan N, Bilgihan A. Leptin and ghrelin levels in patients with obstructive sleep apnea syndrome. Respiration 2005;72:395-401.  Back to cited text no. 32      


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2]

This article has been cited by
1 Liking for high fat foods in patients with Obstructive Sleep Apnoea
Simon S. Smith,Catherine Waight,Geoffrey Doyle,Kalina R. Rossa,Karen A. Sullivan
Appetite. 2014; 78: 185
[Pubmed]
2 Impact of obstructive sleep apnea on the 24-hour metabolic hormone profile
M. Sánchez-de-la-Torre,A. Barceló,J. Piérola,M. de la Peña,J. Valls,F. Barbé
Sleep Medicine. 2014;
[Pubmed]
3 Insights into obstructive sleep apnea research
Mohammad Badran,Najib Ayas,Ismail Laher
Sleep Medicine. 2014;
[Pubmed]
4 Association between continuous positive airway pressure and changes in serum leptin in patients with obstructive sleep apnoea: a meta-analysis
Peiying Zhang,Jianhong Liu,Shengze Long,Xiaomei Xie,Yongzhong Guo
Sleep and Breathing. 2014;
[Pubmed]
5 Ghrelin and its interactions with growth hormone, leptin and orexins: Implications for the sleep-wake cycle and metabolism
García-García, F., Juárez-Aguilar, E., Santiago-García, J., Cardinali, D.P.
Sleep Medicine Reviews. 2014;
[Pubmed]
6 Risk factors for obstructive sleep apnea in non-obese Korean patients: Significance of body weight
Kang Min Park,Kyong Jin Shin,Sam Yeol Ha,JinSe Park,Sungsu Lee,Seungkwon Son,Sung Eun Kim
Sleep and Biological Rhythms. 2014; : n/a
[Pubmed]
7 result 3 Document Effects of nasal continuous positive airway pressure treatment on insulin resistance and ghrelin levels in non-diabetic apnoeic patients with coronary heart disease
Authors of Document Yang, D., Liu, Z.-H., Zhao, Q., Luo, Q.
Chinese Medical Journal. 2013;
[Pubmed]
8 The role of obesity, different fat compartments and sleep apnea severity in circulating leptin levels: the Icelandic Sleep Apnea Cohort study
E S Arnardottir,G Maislin,N Jackson,R J Schwab,B Benediktsdottir,K Teff,S Juliusson,A I Pack,T Gislason
International Journal of Obesity. 2013; 37(6): 835
[Pubmed]
9 Gender-Related Changes of the Epicardial Fat Thickness and Leptin in Obstructive Sleep Apnea
Hakan Akilli,Mehmet Kayrak,Taha Tahir Bekci,Halil Ibrahim Erdogan,Alpay Aribas,Oguzhan Yildirim,Alpaslan Taner,Murat Erer,Ali Unlu
Echocardiography. 2013; : n/a
[Pubmed]
10 Ghrelin and its interactions with growth hormone, leptin and orexins: Implications for the sleep–wake cycle and metabolism
Fabio García-García,Enrique Juárez-Aguilar,Juan Santiago-García,Daniel P. Cardinali
Sleep Medicine Reviews. 2013;
[Pubmed]
11 Stroke and Obstructive Sleep Apnea: A Review
Daniel A. Barone,Ana C. Krieger
Current Atherosclerosis Reports. 2013; 15(7)
[Pubmed]
12 Leptin: A biomarker for sleep disorders?
Weihong Pan,Abba J. Kastin
Sleep Medicine Reviews. 2013;
[Pubmed]
13 result 2 Document The pure effects of obstructive sleep apnea syndrome on cardiac autonomic functions: Heart rate turbulence analysis
Erdem, A., Dogan, O.T., Yontar, O.C., (...), Akkurt, I., Talay, F.
European Review for Medical and Pharmacological Sciences. 2013;
[Pubmed]
14 Plasma ghrelin and pro-inflammatory markers in patients with obstructive sleep apnea and stable coronary heart disease
Yang, D. and Liu, Z. and Luo, Q.
Medical Science Monitor. 2013; 19(1): 251-256
[Pubmed]
15 Sleep and fatigue countermeasures for the neurology resident and physician
Avidan, A.Y.
CONTINUUM Lifelong Learning in Neurology. 2013; 19(1): 204-222
[Pubmed]
16 Neuropharmacology of sleep and wakefulness: 2012 update
Watson, C.J. and Baghdoyan, H.A. and Lydic, R.
Sleep Medicine Clinics. 2012; 7(3): 469-486
[Pubmed]
17 Cardiovascular and metabolic comorbidities in patients with obstructive sleep apnoea syndrome [Comorbiditá cardiovascolare e metabolica nei pazienti affetti da sindrome delle apnee ostruttive del sonno]
Fusetti, M. and Fioretti, A.B. and Valenti, M. and Masedu, F. and Lauriello, M. and Pagliarella, M.
Acta Otorhinolaryngologica Italica. 2012; 32(5): 320-325
[Pubmed]
18 The effect of sleep apnea and insomnia on blood levels of leptin, insulin resistance, IP-10, and hydrogen sulfide in type 2 diabetic patients
Jain, S.K. and Kahlon, G. and Morehead, L. and Lieblong, B. and Stapleton, T. and Hoeldtke, R. and Farrington Bass, P. and Levine, S.N.
Metabolic Syndrome and Related Disorders. 2012; 10(5): 331-336
[Pubmed]
19 result 9 Document Fundamentals of Sleep Medicine (Book )
Authors of Document Berry, R.
. 2012;
[Pubmed]
20 Measuring adiposity in patients: The utility of body mass index (BMI), percent body fat, and leptin
Shah, N.R., Braverman, E.R.
PLoS ONE. 2012; 7(4): art-e33308
[Pubmed]
21 Metabolic syndrome, insulin resistance, fibrinogen, homocysteine, leptin, and C-reactive protein in obese patients with obstructive sleep apnea syndrome
Basoglu, O.K., Sarac, F., Sarac, S., Uluer, H., Yilmaz, C.
Annals of Thoracic Medicine. 2011; 6(3): 120-125
[Pubmed]
22 Type 2 diabetes and pre-diabetes are associated with obstructive sleep apnea in extremely obese subjects: A cross-sectional study
Jan Fredheim,Jan Rollheim,Torbjørn Omland,Dag Hofsø,Jo Røislien,Kristian Vegsgaard,Jøran Hjelmesæth
Cardiovascular Diabetology. 2011; 10(1): 84
[Pubmed]
23 Frequently occurring sleep disorders [Häufige schlafmedizinische erkrankungen]
Mayer, G.
Bundesgesundheitsblatt - Gesundheitsforschung - Gesundheitsschutz. 2011; 54(12): 1284-1295
[Pubmed]
24 Sleep and obesity
Beccuti, G., Pannain, S.
Current Opinion in Clinical Nutrition and Metabolic Care. 2011; 14(4): 402-412
[Pubmed]



 

Top
Print this article  Email this article
 
  Search
 
   Next article
   Previous article 
   Table of Contents
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (433 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
    Methods
    Results
    Discussion
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed4373    
    Printed264    
    Emailed2    
    PDF Downloaded713    
    Comments [Add]    
    Cited by others 24    

Recommend this journal