Annelies Van Eyck1, Kim Van Hoorenbeeck2, Benedicte Y De Winter3, Luc Van Gaal4, Wilfried De Backer5, Stijn L Verhulst2. 1. Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium. Electronic address: Annelies.vaneyck@uantwerpen.be. 2. Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium; Department of Pediatrics, Antwerp University Hospital, Edegem, Belgium. 3. Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium. 4. Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium; Department of Endocrinology, Diabetology and Metabolism, Antwerp University Hospital, Edegem, Belgium. 5. Laboratory of Experimental Medicine and Pediatrics, University of Antwerp, Antwerp, Belgium; Department of Pulmonology, Antwerp University Hospital, Edegem, Belgium.
Abstract
OBJECTIVE: Obstructive sleep apnea (OSA) is common among overweight and obese children, and it is an independent risk factor for developing metabolic syndrome. However, the mechanisms linking OSA and metabolic syndrome are still unclear, but a role for adipose tissue dysfunction caused by intermittent hypoxia has been suggested. Therefore, the goal of this study was to investigate the relationship between OSA and systemic adipokine concentrations in overweight and obese children. METHODS: We included 164 overweight and obese children in a tertiary center and distributed them in groups based on their obstructive apnea-hypopnea index (111 controls, 28 mild OSA, 25 moderate-to-severe OSA). All subjects underwent polysomnography and a blood sample was taken to determine leptin, adiponectin, tumor necrosis factor alpha, and interleukin-6 levels. RESULTS: No significant differences were found in adipokine levels between subjects with or without OSA. Leptin correlated with oxygen desaturation index (r = -0.17, p = 0.03), adiponectin correlated with mean oxygen saturation (r = 0.24, p = 0.002) and with the percentage of sleep time with an oxygen saturation >95% (r = 0.25, p = 0.001). However, these associations did not persist after correction for adiposity. No correlations between interleukin-6 and tumor necrosis factor alpha, and OSA severity were found. CONCLUSION: These results suggest that serum adipokine levels are mostly dependent on central obesity, while they are not influenced by OSA in an obese pediatric population.
OBJECTIVE: Obstructive sleep apnea (OSA) is common among overweight and obesechildren, and it is an independent risk factor for developing metabolic syndrome. However, the mechanisms linking OSA and metabolic syndrome are still unclear, but a role for adipose tissue dysfunction caused by intermittent hypoxia has been suggested. Therefore, the goal of this study was to investigate the relationship between OSA and systemic adipokine concentrations in overweight and obesechildren. METHODS: We included 164 overweight and obesechildren in a tertiary center and distributed them in groups based on their obstructive apnea-hypopnea index (111 controls, 28 mild OSA, 25 moderate-to-severe OSA). All subjects underwent polysomnography and a blood sample was taken to determine leptin, adiponectin, tumor necrosis factor alpha, and interleukin-6 levels. RESULTS: No significant differences were found in adipokine levels between subjects with or without OSA. Leptin correlated with oxygen desaturation index (r = -0.17, p = 0.03), adiponectin correlated with mean oxygen saturation (r = 0.24, p = 0.002) and with the percentage of sleep time with an oxygen saturation >95% (r = 0.25, p = 0.001). However, these associations did not persist after correction for adiposity. No correlations between interleukin-6 and tumor necrosis factor alpha, and OSA severity were found. CONCLUSION: These results suggest that serum adipokine levels are mostly dependent on central obesity, while they are not influenced by OSA in an obese pediatric population.