The Role of Brain-Derived Neurotrophic Factor in Obstructive Sleep Apnea and Endothelial Function in a Pediatric Population With Obesity

Sanae Makhout; Eline Vermeiren; Karolien Van De Maele; Luc Bruyndonckx; Benedicte Y De Winter; Kim Van Hoorenbeeck; Stijn L Verhulst; Annelies Van Eyck

doi:10.3389/fmed.2021.835515

The Role of Brain-Derived Neurotrophic Factor in Obstructive Sleep Apnea and Endothelial Function in a Pediatric Population With Obesity

Front Med (Lausanne). 2022 Jan 20:8:835515. doi: 10.3389/fmed.2021.835515. eCollection 2021.

Authors

Sanae Makhout¹, Eline Vermeiren¹, Karolien Van De Maele^{1

2}, Luc Bruyndonckx^{1

2

3}, Benedicte Y De Winter^{1

4}, Kim Van Hoorenbeeck^{1

2}, Stijn L Verhulst^{1

2}, Annelies Van Eyck^{1

2}

Affiliations

¹ Laboratory of Experimental Medicine and Pediatrics and Member of the Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium.
² Department of Pediatrics, Antwerp University Hospital, Edegem, Belgium.
³ Department of Pediatric Cardiology, Amsterdam University Medical Centers, Amsterdam, Netherlands.
⁴ Department of Gastroenterology and Hepatology, Antwerp University Hospital, Edegem, Belgium.

Abstract

Background: Childhood 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.

Methods: Children 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.

Results: A 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.

Conclusion: BDNF 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.

Keywords: brain-derived neurotrophic factor; endothelial function; multidisciplinary obesity treatment; obstructive sleep apnea; pediatric obesity; weight loss treatment.