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Abstract

Background

Inflammation is involved in the mechanism of obstructive sleep apnoea syndrome (OSAS). Omentin, a newly discovered adipokine, is implicated to play an anti-inflammatory role. This study aims to determine whether serum levels of omentin-1 are associated with the presence and severity of OSAS.

Methods

This study consisted of 192 patients with OSAS and 144 healthy subjects. Serum levels of omentin-1 were measured using enzyme-linked immunosorbent assay.

Results

Serum omentin-1 levels were significantly decreased in OSAS patients compared with healthy controls. Multivariable logistic regression analysis revealed that serum omentin-1 levels were inversely associated with the presence of OSAS (odds ratio 0.520, 95% confidence interval 0.433 to 0.623; P < 0.001). Severe OSAS patients had significantly lower serum omentin-1 levels compared with mild and moderate OSAS patients. Spearman correlation analysis showed that serum omentin-1 levels were correlated with the severity of OSAS. Simple linear regression analysis showed that the serum levels of omentin-1 were negatively correlated with waist circumference, body mass index, systolic blood pressure, homeostasis model assessment of insulin resistance (HOMA-IR), C-reactive protein (CRP), and apnoea-hypopnoea index in patients with OSAS. Furthermore, only HOMA-IR and CRP remained inversely associated with serum omentin-1 after multiple stepwise regression analysis.

Conclusion

Decreased serum omentin-1 levels could be considered as an independent predictive marker of the presence and severity of OSAS.

Introduction

Obstructive sleep apnoea syndrome (OSAS) is a common disorder, with an estimated prevalence of 4% for middle-aged men and 2% for middle-aged women in the general population.¹ It is characterized by repetitive collapse of upper airway during sleep, resulting in impedance to airflow, oxygen desaturation and arousals from sleep.² OSAS could lead to considerable morbidity and mortality. A growing body of evidence indicates that OSAS may be an independent risk factor for insulin resistance, metabolic syndrome, type 2 diabetes and cardiovascular diseases, independently of obesity.³ The exact mechanism of OSAS is not clear. Inflammation is considered to play an important role in the development of OSAS. Recent studies have shown a wide variety of pro-inflammatory mediators are elevated in the circulation of patients with OSAS.⁴

Omentin, a novel adipokine, is produced and secreted mainly by visceral adipose tissue. Omentin, a recently identified fat deposition-specific adipokine coded by two genes (1 and 2), is mainly expressed in visceral omental adipose tissue. Omentin-1 has been shown to be the major circulating isoform in human serum.⁵ Serum omentin-1 level was shown to be significantly decreased in patients with obesity,⁶ polycystic ovary syndrome,⁷ diabetes⁸ and coronary artery disease.⁹ Recent evidence indicates that omentin may serve as an anti-inflammatory mediator. Omentin has been shown to play an anti-inflammatory role by preventing the tumour necrosis factor alpha (TNF-α)-induced COX-2 expression in vascular endothelial cells.¹⁰ Inflammation is associated with the mechanism of OSAS. Therefore, omentin is hypothesized to be involved in the pathophysiology of OSAS.

Although there have been studies on the association of adipokines such as adiponectin,¹¹ leptin,¹² visfatin¹³ and resistin⁴ with OSAS, no investigation on the association between omentin-1 and OSAS has been performed yet. The present study aims to determine the serum levels of omentin-1 in patients with OSAS to assess its role in pathophysiology of OSAS.

Materials and methods

Patients

This study consisted of 192 newly diagnosed male patients with OSAS. All patients with OSAS were diagnosed with polysomnography (PSG). None had undergone any treatment for OSAS. Patients who had personal or family history of psychiatric disorders, history of alcohol and drug abuse, and any other significant medical illnesses such as diabetes mellitus, cancer, cardiovascular, cerebrovascular, pulmonary or neuromuscular disease were excluded from this study. Control participants were recruited from male healthy subjects with medical check-up in the medical checking centre of our hospital and matched to the cases by age, waist circumference (WC) and body mass index (BMI). Subjects with any symptoms of OSAS, history of alcohol and drug abuse, diabetes mellitus, any other respiratory disorder, any malignancy, chronic kidney or liver disease, endocrine disorders or psychiatric disorders were excluded from the control group.

This study was approved by The Ethics Committee of Shengjing Hospital of China Medical University (2010SJH0026), and informed consent was obtained from all participants.

Sleep study

Full PSG monitoring was performed in all participants using the Compumedics E-series Sleep System (Compumedics Sleep: Melbourne, Australia). Polysomnographic monitoring consisted of monitoring of sleep by electroencephalography, electrooculography, electromyography, airflow and respiratory muscle effort, and included measures of electrocardiographic rhythm and blood oxygen saturation. Apneas were defined as a complete lack of air flow for at least 10 s. Hypopnoea was defined as a reduction in airflow with a 50% from baseline for at least 10 s, a 3% drop in oxygen saturation from the preceding stable saturation, and/or arousal. Apnoea-hypopnoea index (AHI) was defined as the frequency of apnoea and hypopnoea per one hour. Subjects with AHI <5 were included in the control group. Subjects with AHI ≥5 were considered to have OSAS. The OSAS patients were then divided into three groups: a mild group with an AHI of ≥5 to <15 (n = 16), a moderate group with an AHI ≥15 to <30 (n = 123) and a severe group with an AHI ≥30 (n = 53).

Measurements

At first examinations, WC and blood pressure were measured. Venous blood was collected after a minimum of 10 h of fasting. Fasting plasma glucose (FPG), serum triglycerides (TG), serum total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) and C-reactive protein (CRP) were tested using an auto biochemistry instrument (Hitachi 7170, Tokyo, Japan). Serum fasting insulin level was tested by radioimmunoassay. Subjects with FPG ≥6.1 to <7.0 mmol/L were diagnosed with impaired fasting glucose (IFG). In addition, subjects with FPG <6.1 mmol/L were diagnosed with normal glucose tolerance (NGT). Serum omentin-1 levels were measured using an enzyme-linked immunosorbent assay (BlueGene Biotech Co., Shanghai, China). BMI was calculated as weight in kilograms divided by height squared in meters (kg/m²). Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated as insulin reading (μIU/mL) multiplied by plasma glucose level (mmol/L) and divided by 22.5.

Statistical analysis

Data are presented as means ± SD or median (interquartile range). Data normality was analysed using the Kolmogorov–Smirnov test. Comparison of the characteristics between patients with OSAS and healthy controls were performed by unpaired t-test or Mann–Whitney U test. Univariate analysis was performed and the variables with a P < 0.10 were then entered into a backward stepwise multivariate logistic regression model to calculate the odds ratio values (ORs) and 95% confidence intervals (CIs) for the presence of OSAS. Kruskal–Wallis test was used to compare the differences of serum omentin-1 levels among mild, moderate and severe OSAS patients. And Nemenyi test was used to compare the differences between each two groups. The correlation of serum omentin-1 levels with the severity of OSAS was determined using Spearman correlation analysis. Mann–Whitney U test was utilized to analyse the differences of serum omentin-1 levels between NGT and IFG subjects. The correlation between serum omentin-1 and other parameters were analysed using simple linear regression analysis. Then a multiple stepwise linear regression analysis was used to determine the contribution of various factors to serum omentin-1. As serum omentin-1 and CRP levels were not normally distributed, logarithmic (log) transformed values were used for multiple linear regression analysis. Statistical analysis was carried out using SPSS version 13.0 software program (SPSS Inc, Chicago, IL, USA). Statistical significance was accepted at a level of P value less than 0.05.

Results

Baseline clinical characteristics

Table 1 shows the clinical and laboratory characteristics of OSAS patients and control subjects. OSAS patients had elevated levels of HOMA-IR and CRP compared with healthy controls. No significant differences were found for age, WC, BMI, systolic blood pressure (SBP), diastolic blood pressure (DBP), FPG, serum TC, TG, LDL-C, HDL-C and statin treatment between the two groups. Sleep characteristics of the two groups are presented in Table 2. OSAS patients showed elevated levels of AHI, the percentage of total sleep time spent with SaO₂ <90% (TST), oxygen desaturation index (ODI), Epworth Sleepiness Score (ESS), as well as decreased levels of average SPO₂ and minimum SPO₂ compared with healthy controls.

Table 1

Clinical and biochemical characteristics of OSAS patients and healthy controls

	OSAS patients	Control	P value
N	192	144
Age (years)	49.24 ± 9.93	48.74 ± 10.62	0.657
WC (cm)	84.93 ± 10.20	85.74 ± 9.66	0.463
BMI (kg/m²)	26.89 ± 3.58	27.14 ± 3.28	0.517
SBP (mmHg)	140.21 ± 13.26	139.48 ± 16.49	0.654
DBP (mmHg)	85.57 ± 11.10	84.86 ± 10.43	0.551
FPG (mmol/L)	5.75 ± 0.74	5.71 ± 0.75	0.566
HOMA-IR	3.11 ± 0.79	2.47 ± 0.76	<0.001
TC (mmol/L)	5.09 ± 1.12	5.07 ± 0.96	0.859
TG (mmol/L)	1.88 ± 0.59	1.87 ± 0.55	0.934
LDL-C (mmol/L)	3.33 ± 0.87	3.36 ± 0.71	0.810
HDL-C (mmol/L)	1.14 ± 0.28	1.16 ± 0.23	0.408
CRP (mg/L)	3.30 (2.30–5.20)	2.30 (1.23–3.20)	<0.001
Omentin-1 (ng/mL)	11.29 (8.02–15.13)	22.62 (18.71–27.21)	<0.001
Statin treatment, n (%)	70 (36.46%)	47 (32.64%)	0.467

OSAS, obstructive sleep apnoea syndrome; WC, waist circumference; BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; HOMA-IR, homeostasis model assessment of insulin resistance; TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; CRP, C-reactive protein

CRP and omentin-1 are given as median (25th–75th percentiles) and other values are given as mean ± SD

The coefficients of variations for the characteristic are as follows:

FPG: 0.176; TC: 0.207; TG: 0.316; LDL-C: 0.341; HDL-C: 0.226; CRP: 0.536; omentin-1: 0.448

Table 2

Sleep characteristics of OSAS patients and healthy controls

	OSAS patients	Control	P
N	192	144
AHI	24.00 (18.00–30.00)	2.00 (1.00–3.00)	<0.001
Average SPO₂ (%)	91.00 (86.25–96.00)	96.00 (92.00–98.00)	<0.001
Minimum SPO₂ (%)	75.00 (63.00–86.75)	89.00 (85.00–93.00)	<0.001
TST (%)	6.96 (2.95/15.07)	0.45 (0.26–0.785)	<0.001
ODI	22.00 (16.00–30.75)	4.00 (1.00–8.00)	<0.001
ESS	13.00 (10.00–17.00)	6.00 (4.00–9.75)	<0.001

OSAS, obstructive sleep apnoea syndrome; AHI, apnoea–hypopnoea index; SPO₂, percentage of oxygen saturation; TST, the percentage of total sleep time spent with SPO₂ <90%; ODI, oxygen desaturation index; ESS, Epworth Sleepiness Score

Values are given as median (25th–75th percentiles)

Serum omentin-1 level in OSAS patients

Serum levels of omentin-1 between OSAS patients and healthy controls are presented in Table 1. Serum omentin-1 levels were significantly decreased in OSAS patients compared with healthy controls (P < 0.001). Simple logistic regression analysis indicated that HOMA-IR (OR 3.732, 95% CI 1.982 to 7.025; P < 0.001), TG (OR 1.404, 95% CI 0.967 to 2.039; P = 0.075), HDL-C (OR 0.159, 95% CI 0.022 to 1.176; P = 0.072), CRP (OR 1.351, 95% CI 1.039 to 1.757; P = 0.025) and omentin-1 levels (OR 0.505, 95% CI 0.416 to 0.614; P < 0.001) showed a trend (P < 0.10) towards an association with the presence of OSAS (Table 3). All these parameters were then entered into a multivariate logistic regression model. Serum omentin-1 levels remained to be inversely associated with the presence of OSAS (OR 0.520, 95% CI 0.433 to 0.623; P < 0.001) (Table 3).

Table 3

Logistic regression analysis for the presence of OSAS

	Simple regression OR (95% CI)	P	Multiple regression OR (95% CI)	P
Age (years)	1.015 (0.972–1.060)	0.498	.	.
WC (cm)	1.018 (0.976–1.061)	0.412
BMI (kg/m²)	0.902 (0.786–1.034)	0.138
SBP (mmHg)	0.977 (0.932–1.024)	0.328
DBP (mmHg)	1.009 (0.946–1.076)	0.791
FPG (mmol/L)	1.155 (0.642–2.078)	0.631
HOMA-IR	3.732 (1.982–7.025)	<0.001	3.233 (1.824–5.731)	<0.001
TC (mmol/L)	1.084 (0.708–1.658)	0.711
TG (mmol/L)	1.404 (0.967–2.039)	0.075	1.409 (0.985–2.015)	0.060
LDL-C (mmol/L)	1.222 (0.611–2.444)	0.571
HDL-C (mmol/L)	0.159 (0.022–1.176)	0.072	0.232 (0.038–1.418)	0.114
CRP (mg/L)	1.351 (1.039–1.757)	0.025	1.352 (1.062–1.720)	0.014
Omentin-1 (ng/mL)	0.505 (0.416–0.614)	<0.001	0.520 (0.433–0.623)	<0.001
Statin treatment, n (%)	1.658 (0.649–4.237)	0.290

Association of omentin-1 levels with OSAS severity

The omentin-1 levels in mild, moderate and severe OSAS patients are displayed in Table 4. Severe OSAS patients showed significantly decreased levels of serum omentin-1 compared with mild and moderate OSAS patients (P = 0.001, 0.014, respectively). However, no differences in serum omentin-1 levels were observed between mild and moderate OSAS patients (P = 0.528). There was a negative correlation between serum omentin-1 levels and the severity of OSAS (r = −0.256, P < 0.001).

Table 4

Association of omentin-1 levels with OSAS severity

	Mild	Moderate	Severe	P	P ₁	P ₂	P ₃
N	16	123	53
Omentin-1 (ng/mL)	12.33 (10.10–14.16)	11.98 (8.42–16.14)	10.20 (6.09–12.43)	<0.001	0.476	<0.001	0.008

OSAS, obstructive sleep apnoea syndrome

Values are given as median (25th–75th percentiles)

P₁: P value between mild OSAS patients and moderate OSAS patients

P₂: P value between mild OSAS patients and severe OSAS patients

P₃: P value between moderate OSAS patients and severe OSAS patients

Omentin-1 levels in NGT and IFG patients with OSAS

The omentin-1 levels in NGT and IFG patients with OSAS are presented in Table 5. IFG patients had decreased levels of omentin-1 compared with NGT patients (P = 0.010).

Table 5

Omentin-1 levels in NGT and IFG subjects with OSAS

	NGT	IFG	P
N	116	76
Omentin-1 (ng/mL)	12.08 (8.44–15.51)	10.35 (6.91–13.54)	0.010

OSAS, obstructive sleep apnoea syndrome; NGT, normal glucose tolerance; IFG, impaired fasting glucose

Values are given as median (25th–75th percentiles)

The association of serum omentin-1 level with other clinical characteristics

Simple linear regression analyses show that serum omentin-1 levels in OSAS patients were negatively correlated with WC, BMI, SBP, HOMA-IR, CRP and AHI (Table 6). Then variables including WC, BMI, SBP, HOMA-IR, CRP and AHI were incorporated into the stepwise linear regression model. Multiple stepwise regression analysis shows that only HOMA-IR (β = 0.202, P = 0.040) and CRP (β = 0.272, P = 0.012) remained to be negatively associated with serum omentin-1.

Table 6

Linear regression analyses between omentin-1 and other clinical parameters

Parameters	r	P
Age (years)	0.042	0.562
WC (cm)	−0.182	0.012
BMI (kg/m²)	−0.174	0.016
SBP (mmHg)	−0.186	0.010
DBP (mmHg)	−0.123	0.090
HOMA-IR	−0.234	0.001
TC (mmol/L)	−0.082	0.256
TG (mmol/L)	−0.098	0.176
LDL-C (mmol/L)	−0.073	0.315
HDL-C (mmol/L)	0.115	0.112
CRP (mg/L)	−0.358	<0.001
AHI	−0.156	0.025
Average SPO₂ (%)	0.076	0.298
Minimum SPO₂ (%)	0.055	0.451
TST (%)	−0.061	0.399
ODI	−0.137	0.058
ESS	−0.102	0.157

WC, waist circumference; BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; HOMA-IR, homeostasis model assessment of insulin resistance; TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; CRP, C-reactive protein; AHI, apnoea–hypopnoea index; SPO₂, percentage of oxygen saturation; TST, the percentage of total sleep time spent with SPO₂ <90%; ODI, oxygen desaturation index; ESS, Epworth Sleepiness Score

Discussion

The current study indicated that serum omentin-1 levels were significantly decreased in OSAS patients compared with healthy subjects. Multivariable logistic regression analysis revealed that serum omentin-1 levels were an independent determinant of the presence of OSAS. Severe OSAS patients had significantly decreased levels of serum omentin-1 compared with mild and moderate OSAS patients. In addition, serum levels of omentin-1 were negatively correlated with WC, BMI, SBP, HOMA-IR, CRP and AHI in patients with OSAS. To the best of our knowledge, there is no previous study evaluating omentin-1 levels in OSAS patients.

Although the main symptom of OSAS is daytime hypersomnolence, OSAS is often complicated with type 2 diabetes mellitus, hypertension and other diseases involving metabolic syndrome.¹⁴ Therefore, it is important to assess the risk of OSAS at an early stage and then to target strategies to prevent or treat OSAS. Our results revealed that serum levels of omentin-1 were significantly decreased in patients with OSAS compared with healthy controls. This indicates that omentin-1 may be involved in the pathophysiology of OSAS. Our results also suggested that omentin-1 levels were negatively correlated with AHI. Severe OSAS patients showed significantly reduced levels of serum omentin-1 compared with mild and moderate OSAS patients. This indicates that decreased omentin-1 levels are associated with the severity of OSAS. Therefore, decreased levels of serum omentin-1 could serve as a new biomarker to predict the presence and severity of OSAS.

Inflammation has been indicated as a potential mechanism for OSAS. Elevated levels of various circulating inflammatory markers, such as tumour necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and CRP have been suggested to be associated with OSAS.¹⁵ Omentin-1, one newly discovered adipokine, is shown to act as an anti-inflammatory mediator. Omentin could inhibit TNF-induced vascular inflammation in human endothelial cells.¹⁰ Omentin was also reported to inhibit TNF-α-induced vascular cell adhesion molecule-1 expression via preventing the activation of p38 and c-Jun N-terminal kinase at least in part through inhibition of superoxide production.¹⁶ These results indicate that omentin may play an important anti-inflammatory role. Furthermore, serum omentin-1 was negatively correlated with TNF-α and IL-6 in patients with type 2 diabetes and polycystic ovary syndrome.^7,17 In both NGT and impaired glucose tolerance subjects, circulating omentin concentration was correlated with CRP and IL-6.¹⁸ Similar results were found in our study, which revealed that serum omentin-1 levels were negatively correlated with CRP. Hence, decreased levels of serum omentin-1 may reflect decreased anti-inflammatory activity and then elevated levels of inflammatory molecules, at last the presence and progression of OSAS.

The current results indicate that serum levels of omentin-1 were negatively correlated with WC, BMI, SBP, and HOMA-IR. This is consistent with other studies. Serum levels of omentin were found to be associated with WC, BMI, SBP and HOMA-IR in patients with obesity,¹⁹ metabolic syndrome (MetS),²⁰ type 2 diabetes¹⁷ and coronary artery disease.²¹ Obesity, insulin resistance and hypertension are multiple compounding factors of MetS. This indicates that omentin-1 may be involved in the mechanism of obesity and MetS. Recent studies have reported decreased concentrations of serum omentin-1 in patients with obesity¹⁸ and MetS.²⁰ Obesity and MetS are closely associated with OSAS. Obesity and particularly central adiposity are potent risk factors for OSAS. In addition, current data suggest that there is an increased prevalence of MetS in subjects with OSAS. This indicates that omentin may be involved in the crosstalk of obesity, MetS and OSAS.

Potential limitations of this study merit consideration. First, the numbers of subjects in the case and control groups were somehow small. Second, this study was cross-sectional, so our findings should be validated in long-term prospective studies.

In conclusion, this study showed that serum omentin-1 levels were decreased in OSAS patients compared with healthy controls. Severe OSAS patients showed significantly decreased levels of serum omentin-1 compared with mild and moderate OSAS patients. Decreased serum omentin-1 levels are suggested to be an independent predictive marker of the presence and severity of OSAS.

Footnotes

DECLARATIONS

Competing interests: All authors have no interests to declare.

Funding: No funding.

Ethical approval: The ethics committee of Shengjing Hospital of China Medical University (2010SJH0026).

Guarantor: XF.

Contributorship: QW, XF researched the literature and conceived the study and they have contributed equally to this article. QW, XF, CZ, PL was involved in protocol development, gaining ethical approval, patient recruitment and data analysis. QW, JK wrote the first draft of the manuscript. All authors reviewed and edited the manuscript and approved the final version of the manuscript.

Acknowledgements: No acknowledgements.

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Decreased levels of serum omentin-1 in patients with obstructive sleep apnoea syndrome

Abstract

Background

Methods

Results

Conclusion

Introduction

Materials and methods

Patients

Sleep study

Measurements

Statistical analysis

Results

Baseline clinical characteristics

Serum omentin-1 level in OSAS patients

Association of omentin-1 levels with OSAS severity

Omentin-1 levels in NGT and IFG patients with OSAS

The association of serum omentin-1 level with other clinical characteristics

Discussion

Footnotes

DECLARATIONS

References