Elevated ghrelin predicts food intake during experimental sleep restriction.

OBJECTIVE: Sleep curtailment has been linked to obesity, but underlying mechanisms remain to be elucidated. This study assessed whether sleep restriction alters 24-h profiles of appetite-regulating hormones ghrelin, leptin, and pancreatic polypeptide during a standardized diet and whether these hormonal alterations predict food intake during ad libitum feeding. METHODS: Nineteen healthy, lean men were studied under normal sleep and sleep restriction in a randomized crossover design. Blood samples were collected for 24 h during standardized meals. Subsequently, participants had an ad libitum feeding opportunity (buffet meals and snacks) and caloric intake was measured. RESULTS: Ghrelin levels were increased after sleep restriction as compared with normal sleep (P < 0.01). Overall, sleep restriction did not alter leptin or pancreatic polypeptide profiles. Sleep restriction was associated with an increase in total calories from snacks by 328 ± 140 kcal (P = 0.03), primarily from carbohydrates (P = 0.02). The increase in evening ghrelin during sleep restriction was correlated with higher consumption of calories from sweets (r = 0.48, P = 0.04). CONCLUSIONS: Sleep restriction as compared with normal sleep significantly increases ghrelin levels. The increase in ghrelin is associated with higher consumption of calories. Elevated ghrelin may be a mechanism by which sleep loss leads to increased food intake and the development of obesity.

Sleep restriction increases free fatty acids in healthy men.

AIMS/HYPOTHESIS: Sleep loss is associated with insulin resistance and an increased risk for type 2 diabetes, yet underlying mechanisms are not understood. Elevation of circulating non-esterified (i.e. free) fatty acid (NEFA) concentrations can lead to insulin resistance and plays a central role in the development of metabolic diseases. Circulating NEFA in healthy individuals shows a marked diurnal variation with maximum levels occurring at night, yet the impact of sleep loss on NEFA levels across the 24 h cycle remains unknown. We hypothesised that sleep restriction would alter hormones that are known to stimulate lipolysis and lead to an increase in NEFA levels. METHODS: We studied 19 healthy young men under controlled laboratory conditions with four consecutive nights of 8.5 h in bed (normal sleep) and 4.5 h in bed (sleep restriction) in randomised order. The 24 h blood profiles of NEFA, growth hormone (GH), noradrenaline (norepinephrine), cortisol, glucose and insulin were simultaneously assessed. Insulin sensitivity was estimated by a frequently sampled intravenous glucose tolerance test. RESULTS: Sleep restriction relative to normal sleep resulted in increased NEFA levels during the nocturnal and early-morning hours. The elevation in NEFA was related to prolonged nocturnal GH secretion and higher early-morning noradrenaline levels. Insulin sensitivity was decreased after sleep restriction and the reduction in insulin sensitivity was correlated with the increase in nocturnal NEFA levels. CONCLUSIONS/INTERPRETATION: Sleep restriction in healthy men results in increased nocturnal and early-morning NEFA levels, which may partly contribute to insulin resistance and the elevated diabetes risk associated with sleep loss.