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Published on: December 6, 2016
DUSP21 expression is associated with obstructive sleep apnea in pediatric patients with obesity
Fabio Affaticati1, Eline Vermeiren2, Pieter Meysman1
1Antwerp Unit for Data Analysis and Computation in Immunology and Sequencing (AUDACIS), University of Antwerp, Antwerp, Belgium; ADReM Data Lab, Department of Mathematics and Computer Science, University of Antwerp, Antwerp, Belgium.
Insights
Children with obesity and obstructive sleep apnea (OSA) have unique gene expression patterns. The gene DUSP21 shows significant changes, suggesting its role in OSA development in obese children.
Area of Science:
- Pediatric Endocrinology
- Sleep Medicine
- Molecular Biology
Background:
- Obesity is a significant risk factor for obstructive sleep apnea (OSA) in children.
- Both obesity and OSA are linked to cardiovascular and metabolic issues through shared pathways.
- Distinguishing individual contributions of obesity and OSA to comorbidities is challenging.
Purpose of the Study:
- To investigate the molecular mechanisms of OSA in obese children.
- To identify distinct gene expression profiles in children with obesity and OSA.
Main Methods:
- Whole blood mRNA sequencing was performed on children with obesity.
- Participants were aged 8-18 years and enrolled in a weight loss program.
- Obstructive sleep apnea (OSA) was diagnosed using polysomnography (oAHI ≥2).
Main Results:
- 10 out of 40 obese children were diagnosed with OSA.
- Differential expression analysis revealed 11 differentially expressed genes (DEGs).
- DUSP21 was significantly downregulated (Log2FoldChange = -7.88, p = 0.0002) in children with OSA.
Conclusions:
- Obese children with OSA display distinct molecular signatures compared to those without OSA.
- The gene DUSP21 may be a key player in the pathophysiology of OSA in this population.
Background:
Obesity is a well-known risk factor for developing obstructive sleep apnea (OSA) in children. Both OSA and obesity are independently associated with cardiovascular and metabolic comorbidities. These comorbidities are driven by shared pathophysiological pathways, making it difficult to distinguish the individual contributions of obesity and OSA. This study aimed to investigate the molecular mechanisms of OSA in children with obesity through whole blood mRNA sequencing.
Methodology:
Children with obesity, aged 8-18 years, were enrolled at the start of a multidisciplinary weight loss treatment in a tertiary hospital. Polysomnography was used to diagnose OSA (oAHI ≥2), and whole blood samples were collected for mRNA sequencing.
Results:
A total of 40 children (mean age 12.4 ± 2.3 years, 57.5 % female) were included, of which 10 patients were diagnosed with OSA. Differential expression analysis identified 11 differentially expressed genes (DEGs) between patients with and without OSA. Seven genes were upregulated (SLC43A3, KLRC3, DAAM2, USP9Y, KDM5D, TTTY15, DBCORP1), while 4 genes were downregulated (DUSP21, XIST, MAP, POLR3D). DUSP21 showed the most significant change, with a Log2FoldChange of -7.88 (p = 0.0002).
Conclusion:
Children with both obesity and OSA exhibit distinct gene expression profiles compared to children with obesity alone. Notably, DUSP21 may play a significant role in the pathophysiological mechanisms of OSA.
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