Salord Neus, Gasa Mercè, Mayos Mercedes, Fortuna-Gutierrez Ana Maria, Montserrat Josep Maria, Sánchez-de-la-Torre Manuel, Barceló Antonia, Barbé Ferran, Vilarrasa Núria, Monasterio Carmen
Sleep Unit, Department of Respiratory Medicine, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain ; Section of Respiratory Medicine, Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Spain ; Universtitat Autonoma de Barcelona, Department of Medicine, Barcelona, Spain ; Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Spain.
Sleep Unit, Department of Respiratory Medicine, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain ; Section of Respiratory Medicine, Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Spain.
J Clin Sleep Med. 2014 Mar 15;10(3):263-70. doi: 10.5664/jcsm.3524.
There is compelling evidence that obstructive sleep apnoea (OSA) can affect metabolic syndrome (MetS) and cardiovascular risk, but the intermediate mechanisms through which it occurs have not been well defined. We explored the impact of OSA in morbidly obese patients with MetS on adipokines, pro-inflammatory markers, endothelial dysfunction, and atherosclerosis markers.
We included 52 morbidly obese patients in an observational study matched for age, gender and central obesity in 3 groups (OSA-MetS, Non-OSA-MetS, and Non OSA-non-MetS). Anthropometrical, blood pressure, and fasting blood measurements were obtained the morning after an overnight polysomnography. VEGF, soluble CD40 ligand (sCD40L), TNF-α, IL-6, leptin, adiponectin, and chemerin were determined in serum by ELISA. OSA was defined as apnea/ hypopnea index ≥ 15 and MetS by NCEP-ATP III.
Cases and control subjects did not differ in age, BMI, waist circumference, and gender (43 ± 10 years, 46 ± 5 kg/m(2), 128 ± 10 cm, 71% females). The cases had severe OSA with 47 (32-66) events/h, time spent < 90% SpO2 7% (5%-31%). All groups presented similar serum cytokines, adipokines, VEGF, and sCD40L levels.
In a morbidly obese population with established MetS, the presence of OSA did not determine any differences in the studied mediators when matched by central obesity. Morbidly obese NonOSA-NonMetS had a similar inflammatory, adipokine VEGF, and sCD40L profile as those with established MetS, with or without OSA. Obesity itself could overwhelm the effect of sleep apnea and MetS in the studied biomarkers.
Salord N; Gasa M; Mayos M; Fortuna-Gutierrez AM; Montserrat JM; Sánchez-de-la-Torre M; Barceló A; Barbé F; Vilarrasa N; Monasterio C. Impact of OSA on biological markers in morbid obesity and metabolic syndrome.
有确凿证据表明阻塞性睡眠呼吸暂停(OSA)会影响代谢综合征(MetS)和心血管风险,但其发生的中间机制尚未明确。我们探讨了OSA对患有MetS的病态肥胖患者的脂肪因子、促炎标志物、内皮功能障碍和动脉粥样硬化标志物的影响。
我们纳入了52例病态肥胖患者进行一项观察性研究,根据年龄、性别和中心性肥胖将其分为3组(OSA-MetS组、非OSA-MetS组和非OSA-非MetS组)。在一夜的多导睡眠监测后的早晨进行人体测量、血压测量和空腹血液检测。通过酶联免疫吸附测定法(ELISA)测定血清中的血管内皮生长因子(VEGF)、可溶性CD40配体(sCD40L)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、瘦素、脂联素和趋化素。OSA定义为呼吸暂停/低通气指数≥15,MetS根据美国国家胆固醇教育计划成人治疗组第三次报告(NCEP-ATP III)来定义。
病例组和对照组在年龄、体重指数(BMI)、腰围和性别方面无差异(43±10岁,46±5kg/m²,128±10cm,71%为女性)。病例组存在严重OSA,呼吸事件为47(32-66)次/小时,血氧饱和度<90%的时间占7%(5%-31%)。所有组的血清细胞因子、脂肪因子、VEGF和sCD40L水平相似。
在已确诊患有MetS的病态肥胖人群中,当按中心性肥胖进行匹配时,OSA的存在并未在所研究的介质中导致任何差异。病态肥胖的非OSA-非MetS组与已确诊患有MetS的人群(无论有无OSA)具有相似的炎症、脂肪因子、VEGF和sCD40L特征。肥胖本身可能掩盖了睡眠呼吸暂停和MetS对所研究生物标志物的影响。
Salord N;Gasa M;Mayos M;Fortuna-Gutierrez AM;Montserrat JM;Sánchez-de-la-Torre M;Barceló A;Barbé F;Vilarrasa N;Monasterio C。OSA对病态肥胖和代谢综合征生物标志物的影响。