Two hormonal systems shift in opposite directions when sleep is restricted. Leptin, released by fat tissue, signals satiety to the hypothalamus and normally rises after a meal; under sleep restriction leptin falls, so the brain receives a weaker "enough" signal. Ghrelin, released by the stomach, signals hunger and normally falls after a meal; under sleep restriction ghrelin rises, so the brain receives a stronger "eat" signal. The combination increases appetite and shifts food preference toward high-calorie, carbohydrate-rich foods.
Glucose handling changes in parallel. After a standardized meal, sleep-restricted subjects show higher blood glucose and a larger insulin response than when fully rested. This means the same amount of glucose requires more insulin to clear, which is reduced insulin sensitivity. The effect is measurable after only a few nights of restricted sleep and is larger when the restriction is combined with a late circadian phase.
These two changes are linked: the same cortisol elevation and sympathetic activation that accompany sleep loss promote hepatic glucose release and oppose insulin action, while the appetite hormone shift increases caloric intake. Together they create a positive energy balance and a higher risk of weight gain over time.