0105 Sleep Restriction Suppresses the Lipemic Response to a Standardized High Fat Dinner in Healthy Young Men

Chronic sleep restriction increases cardiometabolic disease risk, including dyslipidemia. Experimental evidence suggests short-term sleep restriction decreases insulin sensitivity and alters non-esterified fatty acid (NEFA) metabolism. Studies examining the effects of sleep restriction on meal digestion and absorption have focused on changes in glucose and insulin, without assessing the digestion of meal lipids. We assessed the effects of four nights of sleep restriction on lipid transport following a high-fat meal. Fifteen healthy men (mean±SD; age: 22±3 years; BMI: 24.7±3.0 kg/m2) participated in a controlled, 11-day, in-lab sleep restriction protocol. Participants consumed a standardized high-fat dinner (1041kcal; 48.9g fat, 110.5g carbohydrate, 46.6g protein) after two nights of baseline sleep (10h time-in-bed (TIB) opportunity), after four nights of sleep restriction (5h TIB), and after one night of recovery sleep (10h TIB). Frequent blood samples were drawn for five hours following the meal. NEFA and triglycerides (TG) were quantified in triplicate by colorimetric assay (Wako Diagnostics, Infinity, respectively). Sleep restriction decreased TG area under the curve (AUC; minutes 60-300) during the high fat meal by 16.7%±5% (mean±SE; p=0.01). TG AUC fully recovered with one night of recovery sleep (p=0.96). Following sleep restriction, NEFA levels were suppressed throughout the high fat meal procedure (p=0.01), with no time by condition effect (p=0.95). Unlike TG, NEFA remained significantly suppressed after one night of recovery sleep (p=0.01) with an effect of time*condition compared to baseline (p=0.04). Glucose AUC was unaffected by sleep restriction. Compared to baseline, insulin AUC increased with restriction (p=0.004), but did not differ from baseline after recovery sleep (p=0.08). Sleep restriction suppresses postprandial lipemia following a high-fat dinner; these shifts are not fully recovered by one night of sleep extension. The observed changes in the dynamic responses of TG and NEFA levels may be driven by clearance-mediated changes via lipoprotein lipase activation. Compensatory elevations in circulating insulin may be increasing the activation of lipoprotein lipase and enhancing TG and NEFA clearance from the plasma during sleep restriction. UL1TR000127, T32GM108563