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Published on: February 25, 2016
Endothelial dysfunction in obese non-hypertensive children without evidence of sleep disordered breathing
Rakesh Bhattacharjee1, Wadha H Alotaibi, Leila Kheirandish-Gozal
1Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Kentucky, USA.
Insights
Pediatric obesity causes endothelial dysfunction, even without sleep apnea. This early dysfunction in obese children highlights the impact of weight on vascular health.
Area of Science:
- Pediatric Endocrinology
- Cardiovascular Physiology
- Metabolic Disorders
Background:
- Endothelial dysfunction is linked to obesity and obstructive sleep apnea syndrome (OSAS).
- OSAS is common in obese children, but the direct impact of obesity on endothelial function without OSAS is unclear.
- This study investigates endothelial function in obese versus non-obese children, specifically excluding OSAS.
Purpose of the Study:
- To determine if childhood obesity, independent of OSAS, leads to endothelial dysfunction.
- To assess endothelial function in pre-pubertal children with and without obesity.
- To explore the relationship between body fat percentage and endothelial function markers.
Main Methods:
- Recruited pre-pubertal, non-hypertensive children.
- Assessed endothelial function using a modified hyperemic test with arterial occlusion.
- Confirmed absence of OSAS via overnight polysomnography and performed anthropometry.
Main Results:
- Obese children (n=55) showed significantly delayed peak capillary reperfusion compared to non-obese children (n=50).
- No significant differences were found in the magnitude of hyperemia between groups.
- A positive correlation was observed between time to peak reperfusion and body fat percentage (r = 0.365, p < 0.01).
Conclusions:
- Endothelial dysfunction is present in obese children early in life, irrespective of OSAS.
- Mechanisms causing endothelial dysfunction in pediatric obesity are active even without sleep-disordered breathing.
- Findings underscore the vascular risks associated with childhood obesity independent of sleep apnea.
Background:
Endothelial dysfunction is a complication of both obesity and obstructive sleep apnea syndrome (OSAS), the latter being highly prevalent among obese children. It is unknown whether obesity causes endothelial dysfunction in children in the absence of OSAS. This study examines endothelial function in obese and non-obese children without OSAS.
Methods:
Pre-pubertal non-hypertensive children were recruited. Endothelial function was assessed in a morning fasted state, using a modified hyperemic test involving cuff-induced occlusion of the radial and ulnar arteries. The absence of OSAS was confirmed by overnight polysomnography. Anthropometry was also performed.
Results:
55 obese children (mean age 8.6 +/- 1.4 years, mean BMI z-score: 2.3 +/- 0.3) were compared to 50 non-obese children (mean age 8.0 +/- 1.6 years, mean BMI z-score 0.3 +/- 0.9). Significant delays to peak capillary reperfusion after occlusion release occurred in obese compared to non-obese children (45.3 +/- 21.9 sec vs. 31.5 +/- 14.1 sec, p < 0.01), but no differences in the magnitude of hyperemia emerged. Time to peak reperfusion and percentage of body fat were positively correlated (r = 0.365, p < 0.01).
Conclusions:
Our findings confirm that endothelial dysfunction occurs early in life in obese children, even in the absence of OSAS. Thus, mechanisms underlying endothelial dysfunction in pediatric obesity are operational in the absence of sleep-disordered breathing.
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