Abstract
BackgroundChildhood obesity has increased worldwide, becoming a significant public health concern. Brain-derived neurotrophic factor (BDNF) plays an important role in the central regulation of food intake and body weight, but little is known regarding its role in childhood obesity. Next to obesity, BDNF has been linked to obstructive sleep apnea (OSA) and endothelial dysfunction, two obesity-related comorbidities. The aim of this study is to investigate how BDNF, OSA and endothelial dysfunction interact in children with obesity and to determine the effect of weight loss on serum BDNF levels.MethodsChildren and adolescents with obesity aged 8–18 years who were enrolled in a multidisciplinary obesity treatment (MOT) in a tertiary hospital, were prospectively included. Several examinations were conducted during this MOT; at baseline, after 6 months and after 12 months, including the assessment of endothelial function, body composition measurements and a polysomnography. BDNF levels were measured on a serum sample by means of ELISA.ResultsA total of 103 patients with obesity was included, of which 20 had OSA (19.4%). BDNF levels were comparable in children with obesity and OSA and children with obesity but without OSA (26.75 vs. 27.87 ng/ml, p = 0.6). No correlations were found between BDNF and sleep-related variables or between BDNF and endothelial function parameters nor between BDNF and adiposity measures. To investigate if the interaction between OSA and endothelial dysfunction had an influence on BDNF levels, a general linear model was used. This model revealed that a diagnosis of OSA, as well as the interaction between OSA and maximal endothelial dilatation, contributed significantly (p = 0.03, p = 0.04, respectively) to BDNF levels. After 1 year of weight loss therapy, BDNF levels did not change (26.18 vs. 25.46 ng/ml, p = 0.7) in our population.ConclusionBDNF concentrations were comparable in children with obesity, both with and without OSA, indicating that BDNF levels are not affected by OSA. However, we did find an interaction effect of OSA and endothelial function on BDNF levels.
Highlights
The pediatric obesity epidemic has been expanding in both developed and developing countries at an alarming rate over the past decades
No significant differences were found in Brain-derived neurotrophic factor (BDNF) levels between subjects with and without obstructive sleep apnea (OSA) (Figure 1)
Body mass index (BMI), body mass index; BMI z, BMI standard deviation; WHR, waist-to-hip ratio; oAHI, obstructive apnea-hypopnea index; ODI, oxygen desaturation index; TST, total sleep time; TST 95, total sleep time with saturation under 95%; mean SaO2, mean oxygen saturation
Summary
The pediatric obesity epidemic has been expanding in both developed and developing countries at an alarming rate over the past decades. Multiple cardiovascular risk factors are associated with childhood obesity, which can all detrimentally affect the endothelium, leading to endothelial dysfunction [2,3,4], highly prognostic of later cardiovascular morbidity and mortality Another important obesity-related comorbidity is obstructive sleep apnea (OSA) which is characterized by recurrent breathing pauses during sleep. Studies show that the recurrent episodes of arousal and hypoxemia, occurring in OSA patients, can result in increased sympathetic activity, oxidative stress and inflammation, again contributing to endothelial dysfunction [7, 8] This implies that inflammatory processes leading to endothelial dysfunction can play an important role in the association between OSA and cardiovascular disease. The aim of this study is to investigate how BDNF, OSA and endothelial dysfunction interact in children with obesity and to determine the effect of weight loss on serum BDNF levels
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