In contrast to our expectation, short-term sleep loss neither increased food intake nor affected concentrations of the hunger-regulating hormones leptin and ghrelin. However, the observed decrease in daytime physical activity may point to another potentially important behavioral mechanism for the health-impairing influence of sleep loss.

Background: Voluntary sleep restriction is a lifestyle feature of modern societies that may contribute to obesity and diabetes. The aim of the study was to investigate the impact of partial sleep deprivation on the regulation of energy balance and insulin sensitivity. Subjects and Methods: In a controlled intervention, 14 healthy women (age 23–38 years, BMI 20.0–36.6 kg/m²) were investigated after 2 nights of >8 h sleep/night (T0), after 4 nights of consecutively increasing sleep curtailment (7 h sleep/ night, 6 h sleep/night, 6 h sleep/night and 4 h sleep/night; T1) and after 2 nights of sleep recovery (>8 h sleep/night; T2). Resting and total energy expenditure (REE, TEE), glucose-induced thermogenesis (GIT), physical activity, energy intake, glucose tolerance and endocrine parameters were assessed. Results: After a decrease in sleep du-ration, energy intake (+20%), body weight (+0.4 kg), leptin / fat mass (+29%), free triiodothyronine (+19%), free thyroxine (+10%) and GIT (+34%) significantly increased (all p < 0.05). Mean REE, physical activity, TEE, oral glucose tolerance, and ghrelin levels remained unchanged at T1. The effect of sleep loss on GIT, fT3 and fT4 levels was inversely related to fat mass. Conclusion: Short-term sleep deprivation increased energy intake and led to a net weight gain in women. The effect of sleep restriction on energy expenditure needs to be specifically addressed in future studies using reference methods for total energy expenditure.

In comparison with nonobese control subjects, severely obese patients display a marked increase in hedonic hunger that is not observed in patients who have undergone gastric bypass surgery, suggesting that the operation normalizes excessive appetite for palatable foods, which may be an important pathophysiologic feature of severe obesity.

Data indicate an impairment of glucose tolerance after 2 days of sleep restriction to ~4 h that appears to be primarily caused by a reduction in insulin sensitivity. Unchanged HPA secretory activity and IL-6 concentrations argue against a mediation of these effects by stress-related or inflammatory mechanisms.

Data show a marked reduction of the hedonic drive to consume palatable food and beneficial changes in dietary habits characterized by an increased intake of protein-rich foods and vegetables and a reduced consumption of sugar-containing snacks and beverages after RYGB surgery. Based on these findings, it can be speculated that the reduction of the hedonic drive to consume palatable foods induced by RYGB surgery helps severely obese patients to establish healthier dietary habits.