Obstructive sleep apnoea, cigarette smoking and plasma orexin-A in a sleep clinic cohort.

Sleep Disorders Centre, Department of Pulmonology, Atatürk Chest Diseases and Chest Surgery Education and Research Hospital, Ankara, Turkey.
The Journal of international medical research (Impact Factor: 1.1). 03/2009; 37(2):331-40. DOI: 10.1177/147323000903700207
Source: PubMed

ABSTRACT Orexin-A is a neuropeptide involved in the regulation of food intake and the sleep-wake cycle. This study investigated plasma orexin-A levels in a sleep clinic cohort, adjusting for smoking habits, in 76 participants comprising 41 with obstructive sleep apnoea (OSA) (apnoea-hypopnoea index [AHI] 44.1 +/- 19.1 events/h) and 35 without OSA (AHI 6.3 +/- 4.7 events/h). Plasma orexin-A levels were significantly lower in OSA patients (15.0 +/- 4.6 ng/ml) compared with those without OSA (31.4 +/- 6.5 ng/ml). In non-OSA subjects, there was no significant difference between never smokers and ex/current smokers in plasma orexin-A levels (32.9 +/- 9.5 versus 29.7 +/- 8.9 ng/ml, respectively) whereas, in the OSA sub-group, orexin-A levels were significantly lower in never smokers than in ex/current smokers (4.0 +/- 1.2 versus 21.4 +/- 7.0 ng/ml). A significant inverse relationship was found between plasma orexin-A levels and AHI amongst never smokers, but there was no significant relationship amongst ex/current smokers. These results confirm previous studies demonstrating lower levels of plasma orexin-A in OSA patients and indicate that smoking may affect orexin-A levels and AHI.


Available from: Yuksel Peker, Aug 26, 2014
  • [Show abstract] [Hide abstract]
    ABSTRACT: Decreased orexin level has been well demonstrated in patients suffering from narcolepsy, depression accompanied with suicide attempt; obstructive sleep apnea and comorbidity were also demonstrated in these diseases. As C57BL/6J (B6) mice are more "depressed" and have lower brain orexins than A/J mice, B6 mice having chromosome 1 replacement (B6A1 mice) might have restored orexin levels and less depressive behavior. We studied the behavior of 4-6 month old B6, A/J and B6A1 mice with forced swim, tail suspension, and locomotor activity tests. The animals were then sacrificed and hypothalamus and medullas dissected from brain tissue. Orexins-A and -B were determined by radioimmunoassay. Compared with A/J mice, B6 mice displayed several signs of depression, including increased immobility, increased locomotors activity, and decreased orexin A and -B levels in both the hypothalamus and medulla. Compared to B6 mice, B6A1 mice exhibited significantly higher levels of orexins-A and -B in both brain regions. B6A1 mice also exhibited antidepressive features in most of measured variables, including decreased locomotor activity, decreased immobility and increased swim in tail suspension test; compared with B6 mice, however. B6A1 mice also reversed immobility in the early phase of the swim test. In summary, B6 mice exhibited depressive attributes compared with A/J mice, including increased locomotor activity, greater immobility, and decreased brain orexins, these were largely reversed in B6A1 mice. We conclude that orexin levels modulate these B6 behaviors, likely due to expression of A/J alleles on Chromosome 1.
    Journal of Psychiatric Research 08/2014; 59. DOI:10.1016/j.jpsychires.2014.08.008 · 4.09 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective Investigate the clinical features and the blood pressure (BP) pattern of the phenotype of excessive daytime sleepiness (EDS) in OSAHS. Methods A total of 508 Chinese adults with suspected OSAHS were referred to our sleep laboratory from October 2009 to May 2012. On the same night of polysomnography (PSG), the levels of blood pressure were measured before sleeping (bedtime BP) and immediately after waking up in the next morning (morning BP). EDS was recognized as Epworth Sleepiness Scale (ESS)≥9. Subjects were classified into four groups based on the apnea-hypopnea index (AHI) from PSG as follows: control (simple snoring) group (control, n=104) with AHI<5; mild group (mild, n=89) with AHI≥5 and <15; moderate group (moderate, n=70) with AHI≥15 and<30; and severe group (severe, n=245) with AHI ≥30. The differences and correlations between BP and PSG parameters in EDS and non-EDS group of OSAHS patients were analyzed. Results In all subjects, ESS was positively correlated with morning diastolic blood pressure (DBP), Mean arterial pressure (MAP) and bedtime DBP (r=0.144, 0.102 and 0.114, respectively, each P value<0.05). In OSAHS patients, ESS was only positively correlated with morning DBP (r=0.137, P<0.05). OSAHS patients with EDS phenotype were younger and were more likely to have the symptom of waking up feeling tired (36.1% vs. 23.2%, p=0.023), who had lower MSaO2, longer SIT90 (the ratio of time of SpO2 below 90% in total sleep time) and higher DBP (bedtime as well as morning). In patients with AHI≥15, ESS was correlated positively with both bedtime and morning DBP after controlling the confounding effects of age, sex, BMI, AHI and nadir nocturnal oxygen saturation( r=0.126,0.143, respectively, both P values<0.05). And in OSAHS patients of EDS phenotype, the bedtime DBP, bedtime MAP, morning DBP, and morning MAP were 3~5 mm Hg higher than that in patients of non-EDS phenotype(P<0.05). In the moderate and severe OSAHS group, patients with EDS phenotype were younger and had a lower mean blood oxygen saturation (MSaO2), longer time of SpO2 below 90% and higher SIT90 than patients with non-EDS phenotype (P<0.05). In hypertensive OSAHS patients, patients with EDS were also younger and had higher micro-arousal index (MiI), as well as higher morning DBP, morning MAP and bedtime DBP than that in non-EDS group (P<0.05). Conclusions EDS in OSAHS patients is a special phenotype, which was characterized by younger age, higher DBP and more severe hypoxic load. This feature is mainly manifested in moderate and severe OSAHS patients. It is very important to identify the phenotype of EDS in patients with OSAHS, who may meet more benefits from effective treatment of OSAHS by correcting the intermittent nocturnal hypoxia and sleep fragmentation.
    International journal of medical sciences 01/2014; 11(7):713-20. DOI:10.7150/ijms.7487 · 1.55 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: This review summarizes data regarding the brain expression of the orexin (hypocretin) system including: prepro-orexin (PPO), orexin A (OxA), orexin B (OxB) and the two orexin receptors 1 and 2 (OxR1, OxR2). Clinical data is limited to OxA and OxB in cerebral spinal fluid and serum/plasma, thus necessitating the development of animal models to undertake mechanistic studies. We focus on changes in animal models that were either exposed to a regime of altered sleep, metabolic energy homeostasis, exposed to drugs and noxious insults. Many more expressional studies are available for PPO, OxA and OxB levels, compared to studies of the receptors. Interestingly, the direction and pattern of change for PPO, OxA and OxB is inconsistent amongst studies, whereas for the receptors, there tends to be increased expression for both OxR1 and OxR2 after alterations in energy homeostasis, and an increased expression after noxious insults or exposure to some drugs. The clinical implications of these results from animal models are discussed in light of the findings from human studies, and future research directions are suggested to fill knowledge gaps with regard to the orexin system, particularly during early brain development.
    Brain research 07/2013; DOI:10.1016/j.brainres.2013.06.035 · 2.83 Impact Factor