[Exercise capacity in children with mild sleep-disordered breathing]. / Capacité physique de l'enfant présentant un syndrome d'apnée du sommeil léger.

INTRODUCTION: While the association between sleep-disordered breathing (SDB) and low physical activity has been reported in children, little information is available on the impact of SDB on exercise capacity. The aim of this study was to assess exercise capacity in children with SDB in order to estimate the relevance of exercise training intervention. METHODS: Twelve young patients with suspected SDB matched with 11 presumably healthy subjects of same age range (aged 13±0.5yr) were investigated. Both groups underwent physical activity assessment, full night polysomnography, incremental and all-out exercise tests. RESULTS: The respiratory disturbance index was higher in the patient group (4.6±4.7 vs 0.8±0.6; P=0.02). Children with SDB had lower VO2max (32.0±9.9 vs 42.3±5.7mL.kg-1.min-1, P=0.007) and lower peak power (8.6±3.4 vs 11.8±1.9W.kg-1, P=0.009). A significant correlation between VO2max and weekly physical activity only was found in the SDB group (P=0.005). CONCLUSION: Mild SDB may be associated with impairment of both aerobic and anaerobic exercise capacity in children, related to poor physical activity. Exercise training could bring clinical benefit in this population.

Subtle metabolic and liver gene transcriptional changes underlie diet-induced fatty liver susceptibility in insulin-resistant mice.

AIMS/HYPOTHESIS: Complex changes in gene expression are associated with insulin resistance and non-alcoholic fatty liver disease (NAFLD) promoted by feeding a high-fat diet (HFD). We used functional genomic technologies to document molecular mechanisms associated with diet-induced NAFLD. MATERIALS AND METHODS: Male 129S6 mice were fed a diet containing 40% fat (high-fat diet, HFD) for 15 weeks. Glucose tolerance, in vivo insulin secretion, plasma lipid profile and adiposity were determined. Plasma metabonomics and liver transcriptomics were used to identify changes in gene expression associated with HFD-induced NAFLD. RESULTS: In HFD-fed mice, NAFLD and impaired glucose and lipid homeostasis were associated with increased hepatic transcription of genes involved in fatty acid uptake, intracellular transport, modification and elongation, whilst genes involved in beta-oxidation and lipoprotein secretion were, paradoxically, also upregulated. NAFLD developed despite strong and sustained downregulation of transcription of the gene encoding stearoyl-coenzyme A desaturase 1 (Scd1) and uncoordinated regulation of transcription of Scd1 and the gene encoding sterol regulatory element binding factor 1c (Srebf1c) transcription. Inflammatory mechanisms appeared to be stimulated by HFD. CONCLUSIONS/INTERPRETATION: Our results provide an accurate representation of subtle changes in metabolic and gene expression regulation underlying disease-promoting and compensatory mechanisms, collectively contributing to diet-induced insulin resistance and NAFLD. They suggest that proposed models of NAFLD pathogenesis can be enriched with novel diet-reactive genes and disease mechanisms.