Gut Hormones and Appetite Control Basics

Exploring the hormonal signals that influence hunger and satiety through the gut-brain axis.

The Gut-Brain Axis

Communication between the digestive system and the brain involves multiple signaling pathways—hormonal, neural, and immune. This bidirectional system, called the gut-brain axis, integrates signals about nutrient status and digestive state to influence appetite, satiety, and eating behaviour.

Ghrelin: The Hunger Hormone

Ghrelin is produced primarily by cells in the stomach and increases before meals, signaling the brain that energy is needed. Blood ghrelin levels typically rise during fasting periods and decrease after eating. Ghrelin influences not only appetite but also metabolic rate and reward responses to food.

Factors that influence ghrelin include meal timing, sleep quality, stress levels, and overall energy status. Adequate sleep, for example, supports more stable ghrelin patterns, whereas sleep deprivation may increase ghrelin signaling.

Leptin: The Satiety Signal

Leptin is produced by adipose (fat) tissue and signals the brain about long-term energy stores. Higher leptin levels typically reduce appetite and increase energy expenditure. This hormone communicates to the hypothalamus that adequate energy reserves exist.

However, in conditions of chronic overnutrition, leptin resistance can develop—meaning that despite high leptin levels, the brain does not respond appropriately to satiety signals. This represents a dysregulation of the hormone signaling system rather than a simple hormone deficiency.

Other Appetite-Regulating Hormones

Beyond ghrelin and leptin, multiple hormones influence appetite and energy regulation. Peptide YY (PYY) and GLP-1 (Glucagon-like peptide 1) are released from intestinal cells in response to nutrient intake and promote satiety. CCK (Cholecystokinin) is released in response to fat and protein and influences meal termination.

Nutrient Composition Effects

Different macronutrients trigger different hormonal responses. Protein consumption, for example, elicits greater PYY and GLP-1 release compared to carbohydrates, which may contribute to protein's satiating effects. Dietary fat influences CCK release and can affect satiety duration.

This means that the nutritional composition of meals influences not only energy content but also hormonal signaling that affects subsequent hunger and food intake patterns.

Timing and Circadian Patterns

Appetite hormones follow circadian (daily) patterns. Ghrelin typically increases in the evening and early morning, reflecting evolutionary patterns of food seeking and eating. These patterns can be influenced by meal timing, light exposure, and sleep schedules.

Stress and Cortisol

Chronic stress and elevated cortisol can alter the ghrelin-leptin balance, potentially increasing appetite and affecting food choice patterns. Stress responses involve multiple neural and hormonal pathways that can override satiety signals.