Fat accumulation, leptin, and hypercapnia in obstructive sleep apnea-hypopnea syndrome
Department of Respirology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba 260-8670, Japan. Chest
(Impact Factor: 7.48).
02/2005; 127(2):543-9. DOI: 10.1378/chest.127.2.543
Obesity and visceral fat accumulation (VFA) are risk factors for the development of obstructive sleep apnea-hypopnea syndrome (OSAHS), and a subgroup of OSAHS patients acquire hypoventilation. Circulating leptin, an adipocyte-derived signaling factor, increases in accordance with body mass index (BMI); under experimental conditions, leptin selectively decreases visceral adiposity and it is also a respiratory stimulant.
To investigate whether the location of body fat deposits, ie, the distribution of VFA and subcutaneous fat accumulation (SFA), contributes to hypoventilation and whether circulating levels of leptin are involved in the pathogenesis of hypoventilation, which is often observed in OSAHS.
We assessed VFA and SFA by abdominal CT scan, and measured lung function and circulating levels of leptin in 106 eucapnic and 79 hypercapnic male patients with OSAHS.
In the whole study group, circulating leptin levels correlated with BMI (r = 0.56), VFA (r = 0.24), and SFA (r = 0.47), but not with Po(2) or sleep mean arterial oxygen saturation (Sao(2)). BMI, percentage of predicted vital capacity, FEV(1)/FVC ratio, apnea-hypopnea index, sleep mean Sao(2), VFA, and SFA were not significantly different between two groups. Circulating leptin levels were higher in the hypercapnic group than in the eucapnic group. Logistic regression analysis indicated that serum leptin was the only predictor for the presence of hypercapnia (beta = 0.21, p < 0.01).
These results suggest that the location of body fat deposits may not contribute to the pathogenesis of hypoventilation, and circulating leptin may fail to maintain alveolar ventilation in hypercapnic patients with OSAHS.
Available from: del Campo F Felix
- "Several studies have shown increased levels of leptin in OSAS (Phillips et al., 2000; Tokuda et al., 2008), suggesting its role in the disease (Ip et al., 2000). The mechanisms underlying the relation between leptin and OSAS are very diverse, and may involve overnight changes in apnea levels (Patel et al., 2004; Sanner et al., 2004), sleep hypoxemia (Tatsumi et al., 2005), and hypercapnia (Shimura et al., 2005). "
Cardiovascular Risk Factors, 03/2012; , ISBN: 978-953-51-0240-3
Available from: Mehmet Karadag
- "It was suggested that sleep hypoxemia may be the main determinant of circulating leptin levels. Shimura et al. demonstrated that circulating leptin levels correlated with BMI, VFA, and SFA, but not with PaO2 or sleep mean arterial oxygen saturation. They reported that leptin levels were higher in the hypercapnic group than in the eucapnic group. "
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ABSTRACT: The aim of this study was to investigate the relationship among plasma leptin, ghrelin, adiponectin, resistin levels, and obstructive sleep apnea syndrome (OSAS).
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.
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.
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.
07/2010; 5(3):161-5. DOI:10.4103/1817-1737.65050
Available from: Kamyar Ghabili
- "), anti-diuretic hormone (vasopressin) (Raff et al., 1983), noradrenaline and prolactin (Kaye et al., 2004; Rojas Vega et al., 2003), glucagon (Bloom et al., 1977) and oxytocin and growth hormone (Leach and Forsling, 2004), and also activation of the renin-angiotensin-aldosterone (Raff and Jankowski, 1993; Raff et al., 1984; Raff and Roarty, 1988) and HPA (Bloom et al., 1977; Argyropoulos et al., 2002) axes. Circulating leptin concentrations are higher in hypercapnic than in eucapnic patients with obesity or obstructive sleep apnea (Phipps et al., 2002; Shimura et al., 2005). It has been shown that plasma ACTH and corticosteroid levels are higher during hypercapnia (PaCO 2 of 59 mm Hg) at all levels of PaO 2 ranging from 26 to 88 mm Hg (Raff et al., 1983). "
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ABSTRACT: Carbon dioxide (CO(2)) interacts in complex ways with the brain and the endocrine and immune systems. Arterial CO(2) may be elevated or decreased following cerebral ischemia-reperfusion injury or stroke. The aim of the present review is to delineate potential changes in the neuroimmunoendocrine system following cerebral ischemia-reperfusion injury and to provide evidence for the modulatory role of carbon dioxide in this setting. It appears that lesions of the right and left cerebral hemispheres are associated with different patterns of immune activation and cytokine release. Changes in arterial CO(2) can profoundly alter the neuroimmunoendocrine system, especially the hypothalamic-pituitary-adrenal (HPA) axis and the production of pro-inflammatory cytokines. Hypercapnia activates the HPA axis, exerts antiinflammatory and antioxidant effects, and can alter the secretion and function of various brain neurotransmitters. There is conflicting evidence surrounding arterial CO(2): its effects on the ischemic brain may be either beneficial or deleterious. Mild hypercapnia may exert some neuroprotection following cerebral ischemia, but severe hypercapnia may aggravate neuronal injury by extra- and intra-cellular acidification and/or impairment of cellular calcium hemostasis. Future studies are required to delineate the potential relationship between arterial CO(2) and prognosis and long-term survival following cerebral ischemia-reperfusion injury. "Therapeutic hypercapnia" seems to be a promising approach to the treatment of stroke patients, and its use should be justified by further experimental and clinical studies.
Life Sciences 10/2008; 83(11-12):381-7. DOI:10.1016/j.lfs.2008.07.007 · 2.70 Impact Factor
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