Metabolic alterations and systemic inflammation in obstructive sleep apnea among nonobese and obese prepubertal
David Gozal1, Oscar Sans Capdevila, Leila Kheirandish-Gozal
1Kosair Children's Hospital Research Institute, University of Louisville, 570 South Preston Street, Suite 204, Louisville, KY 40202, USA. david.gozal@louisville.edu
Insights
Obstructive sleep apnea (OSA) in children is linked to metabolic issues, especially in obese youth. Treating OSA improves lipid profiles and reduces inflammation, suggesting a key role in metabolic health.
Area of Science:
- Pediatric Endocrinology
- Sleep Medicine
- Metabolic Syndrome
Background:
- Obstructive sleep apnea (OSA) is linked to metabolic syndrome in adults, but its role in prepubertal children is less clear.
- Metabolic derangements associated with OSA appear less pronounced in prepubertal children compared to adults.
Purpose of the Study:
- To investigate the mechanistic role of OSA in metabolic regulation in prepubertal children.
- To assess the impact of adenotonsillectomy on metabolic parameters in children with OSA.
Main Methods:
- Sixty-two children with OSA (obese and nonobese) underwent polysomnography.
- Fasting glucose, insulin, C-reactive protein, apolipoprotein B, and lipid profiles were measured before and after adenotonsillectomy.
Main Results:
- Adenotonsillectomy improved sleep quality in children with OSA.
- Nonobese children showed improved lipid profiles and reduced inflammation markers post-surgery.
- Obese children experienced significant improvements in lipid profiles, C-reactive protein, and apolipoprotein B after adenotonsillectomy.
Conclusions:
- OSA plays a significant role in metabolic dysregulation in obese children.
- Treatment of OSA improves lipid homeostasis and systemic inflammation, independent of obesity levels.
- OSA does not appear to induce insulin resistance in nonobese pediatric patients.
Rationale:
Obstructive sleep apnea (OSA) has been associated with a higher prevalence and severity of the metabolic syndrome in adult patients, even after controlling for obesity. In contrast, OSA in prepubertal children does not appear to correlate with the magnitude of such metabolic derangements.
Objectives:
To further establish the potential mechanistic role of OSA in metabolic regulation in prepubertal children.
Methods:
Fasting glucose, insulin, C-reactive protein, apolipoprotein B, and serum lipid concentrations were determined during the initial polysomnographic diagnosis of OSA and 6-12 months after adenotonsillectomy in both obese and nonobese children.
Measurements And Main Results:
Sixty-two children with OSA (37 obese and 25 nonobese), age 7.40 +/- 2.6 years (mean +/- SD) completed the study. After adenotonsillectomy, significant improvements in apnea-hypopnea index and sleep fragmentation occurred, particularly among nonobese children. In nonobese children, adenotonsillectomy was associated with mild increases in body mass index z scores, no changes in either fasting glucose or insulin, significant increases in high-density lipoprotein and reciprocal decreases in low-density lipoprotein, and reductions in plasma C-reactive protein and apolipoprotein B levels. In obese children, adenotonsillectomy did not result in body mass index or glucose changes, but was associated with marked improvements in all other measures.
Conclusions:
OSA does not appear to induce insulin resistance in nonobese pediatric patients but seems to play a significant role in obese patients. The significant improvements in lipid profiles, C-reactive protein, and apolipoprotein B after adenotonsillectomy in the two groups suggest a pathogenic role for OSA in lipid homeostasis and systemic inflammation independent of the degree of adiposity.
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