SAT-251 Acute Sleep Change, Laboratory Meal Energy Intake, and Insulin Sensitivity in Children

Background Many studies show a correlation between short sleep duration and obesity/insulin resistance. One hypothesis for this association is that shortened sleep causes increased energy intake (EI). In some studies, experimentally reduced sleep duration has been found to increase total EI. There are mixed findings about the effects of habitual and acute short sleep on the macronutrient content of consumed meals. Additionally, there are few pediatric studies with objectively measured sleep duration (e.g. using actigraphy). Therefore, we aimed to determine if an acute sleep change was associated with greater total EI, altered macronutrient intake, or altered insulin sensitivity in children. Methods Healthy weight and overweight volunteers (n=18, 44% male), aged 7-11 years wore ActiGraph activity monitors for six consecutive 24 hour periods to determine nightly sleep duration. Volunteers were given no direction regarding sleep for the week. On day six, children underwent a standardized oral glucose tolerance test (OGTT) (1.75g/kg, max 75g) after which total EI (kcal) and macronutrient composition (% of total EI) were measured during a lunchtime laboratory test meal (>10,000 kcal; ~12% protein, 32% fat, 56% CHO). Subjects were directed to eat as much as they wanted. Acute change in sleep was calculated by subtracting each participant’s average nightly total sleep time over the entire week from their total sleep time on the fifth night (i.e., night before the test meal). Linear regressions examined associations of acute change in sleep with insulin AUC during OGTT, total EI, % CHO, % fat, and ratio of %CHO to %fat intake. Results Controlling for daily predicted energy needs and physical activity level, acute change in sleep (mean of 27.5 minutes less than average) was not significantly associated with total EI (p=0.58). However, the %CHO trended toward a significant negative correlation (r=-0.47, p=0.05) and %fat was positively associated (r=0.50, p=0.036) with acute change in sleep such that the %CHO to %fat intake ratio was greater in those with greater sleep deficit (p=0.039). Additionally, controlling for BMI-z score, basal insulin, and age, greater sleep deficit was associated with increased insulin AUC during the OGTT (p=0.001). Discussion Contrary to some previous experimental data, acute sleep deficit had no significant association with total EI; however, acute sleep deficit was associated with increased relative carbohydrate intake. Acute sleep deficit was also associated with decreased relative fat intake, a known satiating macronutrient. These data also suggest an acute decrease in insulin sensitivity associated with sleep deficit. All three mechanisms could explain or exacerbate the increased prevalence of obesity and metabolic abnormalities in children with short sleep duration and therefore, provide support for sleep-associated adjunctive treatment for such children.