Introduction: 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 pre-pubertal children does not appear to correlate with the magnitude of such metabolic derangements. Methods: To further establish the potential mechanistic role of OSA in metabolic regulation in pre-pubertal children, 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 non-obese children. Results: Sixty-two children with OSA (37 obese and 25 non-obese) with a mean age 7.40±2.6 years [SD] completed the study. After adenotonsillectomy, significant improvements in apnea-hypopnea index and sleep fragmentation occurred, particularly among non-obese children. In non-obese 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 non-obese pediatric patients but seems to play a significant role in obese patients. The significant improvements in lipid profiles, C-reactive protein, and apolipoprotein B followingadenotonsillecotmy in the 2 groups suggest a pathogenetic role for OSA in lipid homeostasis and systemic inflammation independently from the degree of adiposity.