Abstract
BackgroundEndothelial 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.MethodsPre-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.Results55 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).ConclusionsOur 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.
Highlights
Endothelial dysfunction is a complication of both obesity and obstructive sleep apnea syndrome (OSAS), the latter being highly prevalent among obese children
Obesity in children has nearly doubled over the past 2 decades in the United States, with approximately 15% of all children fulfilling obesity criteria, i.e., a body mass index (BMI) over the 95th percentile on standard growth curves assembled by the Centers for Disease and
Delays in vascular reperfusion kinetics suggest that the integrity of the vasculature that is critical for adequate responses to vasodilatory stimuli, such as those operating in post-ischemic recovery responses, is significantly compromised in obese children, and that such impairments are correlated to the degree of dyslipidemia and percent body fat
Summary
Endothelial dysfunction is a complication of both obesity and obstructive sleep apnea syndrome (OSAS), the latter being highly prevalent among obese children. Obesity has been associated with an increase in the prevalence of diabetes mellitus, dyslipidemia, hypertension, and potentially leads to the development of the metabolic syndrome and cardiovascular disease [1,2]. As a consequence of the increasing rates of childhood obesity, and the above-listed obesityassociated co-morbidities, the global life expectancy in the United States is expected to decline, [8,9,10] and has led to the American Heart Association as well as the American Diabetes Associations both to re-classify obesity as a ‘major, modifiable risk factor’ for cardiovascular disease [11]. Systemic hypertension in children is rare with an estimated prevalence at 2-5%,
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