Impact of OSA on Biological Markers in Morbid Obesity and Metabolic Syndrome
1Sleep Unit, Department of Respiratory Medicine, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain; 2Section of Respiratory Medicine, Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Spain; 3Universtitat Autonoma de Barcelona, Department of Medicine, Barcelona, Spain; 4Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Spain; 5Sleep Unit, Department of Respiratory Medicine, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; 6Sleep Unit, Department of Respiratory Medicine, Hospital Clinic de Barcelona, Barcelona, Spain; 7Respiratory Diseases Research Unit, Hospital Universitari Arnau de Vilanova, IRB Lleida Lleida, Spain; 8Clinic Analysis Service, Hospital Universitari Son Espases, Palma de Mallorca, Spain; 9Department of Endocrinology and Nutrition, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain; 10CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain
Background and Objective:
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/m2, 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. J Clin Sleep Med 2014;10(3):263-270.
Please login to continue reading the full article
Subscribers to JCSM get full access to current and past issues of the JCSM.
Login to JCSM
Not a subscriber?
Join the American Academy of Sleep Medicine and receive a subscription to JCSM with your membership