INTRODUCTION: Obstructive sleep apnea (OSA) has been implicated in the pathophysiology of metabolic syndrome. Its contribution to insulin resistance is complicated by obesity and puberty. We hypothesized that OSA is associated with worse insulin resistance and lower adiponectin after adjustment for obesity and puberty and that catecholamines might mediate these changes. METHODS: Normal controls and children with suspected OSA were recruited and categorized as pubertal or prepubertal. Overnight polysomnography (PSG) was performed. Subjects were categorized as OSA for total apnea hypopnea index (Total-AHI) > or = 1.5 events/h. Fasting blood glucose, insulin, adiponectin, and 24-hour urinary catecholamines were obtained. Homeostatic model assessment of insulin resistance (HOMA) was calculated. The independent effects of OSA upon HOMA, adiponectin, and urinary catecholamines following adjustment for body mass index (BMI) were determined. RESULTS (median; min, max): Subjects (n = 98, 42F; 11 +/- 4 years, 37 prepubertal) were generally overweight (BMI-Z = 2.1; -3, 4.1) and had wide-ranging insulin sensitivities (HOMA = 2.7; 0.5, 27) and PSG parameters (Total-AHI = 1.6; 0, 185). The risks of elevated insulin (P = 0.04) and HOMA (P = 0.05) were higher in OSA vs non OSA obese pubertal children. Polysomnographic markers of OSA, including Total-AHI (P = 0.001, R2 = 0.32), were negatively associated with adiponectin in pubertal children. Total-AHI and oxygen desaturation were associated with higher urinary normetanephrine and norepinephrine. CONCLUSIONS: In obese pubertal children, OSA was associated with worse insulin resistance. Worsening OSA was associated with lower adiponectin and increasing urinary catecholamines. Whether OSA directly lowers adiponectin and aggravates a predisposition to insulin resistance is unknown, but these preliminary findings highlight the importance of further studying pediatric OSA.
INTRODUCTION:Obstructive sleep apnea (OSA) has been implicated in the pathophysiology of metabolic syndrome. Its contribution to insulin resistance is complicated by obesity and puberty. We hypothesized that OSA is associated with worse insulin resistance and lower adiponectin after adjustment for obesity and puberty and that catecholamines might mediate these changes. METHODS: Normal controls and children with suspected OSA were recruited and categorized as pubertal or prepubertal. Overnight polysomnography (PSG) was performed. Subjects were categorized as OSA for total apnea hypopnea index (Total-AHI) > or = 1.5 events/h. Fasting blood glucose, insulin, adiponectin, and 24-hour urinary catecholamines were obtained. Homeostatic model assessment of insulin resistance (HOMA) was calculated. The independent effects of OSA upon HOMA, adiponectin, and urinary catecholamines following adjustment for body mass index (BMI) were determined. RESULTS (median; min, max): Subjects (n = 98, 42F; 11 +/- 4 years, 37 prepubertal) were generally overweight (BMI-Z = 2.1; -3, 4.1) and had wide-ranging insulin sensitivities (HOMA = 2.7; 0.5, 27) and PSG parameters (Total-AHI = 1.6; 0, 185). The risks of elevated insulin (P = 0.04) and HOMA (P = 0.05) were higher in OSA vs non OSA obese pubertal children. Polysomnographic markers of OSA, including Total-AHI (P = 0.001, R2 = 0.32), were negatively associated with adiponectin in pubertal children. Total-AHI and oxygen desaturation were associated with higher urinary normetanephrine and norepinephrine. CONCLUSIONS: In obese pubertal children, OSA was associated with worse insulin resistance. Worsening OSA was associated with lower adiponectin and increasing urinary catecholamines. Whether OSA directly lowers adiponectin and aggravates a predisposition to insulin resistance is unknown, but these preliminary findings highlight the importance of further studying pediatric OSA.
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