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The Role of Brain-Derived Neurotrophic Factor in Obstructive Sleep Apnea and Endothelial Function in a Pediatric
Sanae Makhout1, Eline Vermeiren1, Karolien Van De Maele1,2
1Laboratory of Experimental Medicine and Pediatrics and Member of the Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium.
Insights
Brain-derived neurotrophic factor (BDNF) levels are not directly affected by obstructive sleep apnea (OSA) in obese children. However, OSA and endothelial dysfunction interact to influence BDNF levels, independent of weight loss.
Area of Science:
- Pediatric Endocrinology
- Neuroscience
- Public Health
Background:
- Childhood obesity is a global health crisis.
- Brain-derived neurotrophic factor (BDNF) influences appetite and weight regulation.
- BDNF is linked to obstructive sleep apnea (OSA) and endothelial dysfunction, common in obese children.
Purpose of the Study:
- To examine the interplay between BDNF, OSA, and endothelial dysfunction in obese children.
- To assess the impact of weight loss on serum BDNF levels.
Main Methods:
- Prospective study of 103 obese children (8-18 years) in a multidisciplinary obesity treatment program.
- Evaluations included endothelial function, body composition, polysomnography, and serum BDNF measurement (ELISA) at baseline, 6, and 12 months.
- General linear models analyzed the interaction effects.
Main Results:
- Obese children with and without OSA showed comparable BDNF levels (26.75 vs. 27.87 ng/ml).
- No correlations found between BDNF and sleep variables, endothelial function, or adiposity.
- OSA diagnosis and its interaction with maximal endothelial dilatation significantly influenced BDNF levels (p=0.03, p=0.04).
- BDNF levels remained unchanged after 1 year of weight loss therapy (p=0.7).
Conclusions:
- Serum BDNF levels in obese children are not directly influenced by the presence of OSA.
- An interaction between OSA and endothelial function significantly affects BDNF levels in this population.
- Weight loss therapy did not alter BDNF concentrations after one year.
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.
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