Satiety Hormones Explained

Appetite and satiety are regulated by a complex system of hormonal signals. Understanding these signals provides insight into how the body regulates food intake and energy balance.

The Satiety System

The regulation of appetite and fullness is not controlled by a single hormone, but rather by an integrated system involving multiple hormonal signals, neurological pathways, and sensory inputs. This system communicates between the digestive tract, adipose tissue, and the brain, coordinating energy intake with energy needs.

Leptin

Leptin is produced by adipose tissue and signals energy sufficiency to the brain. It suppresses appetite and increases energy expenditure when energy stores (body fat) are adequate. Conversely, leptin levels decrease during energy restriction or weight loss, increasing appetite signals and promoting food-seeking behaviour. However, in individuals with elevated body fat, leptin resistance can occur, where despite high leptin levels, the brain does not receive the satiety signal effectively. This creates a mismatch between actual energy stores and perceived sufficiency.

Ghrelin

Ghrelin is produced primarily by the stomach and is sometimes called the "hunger hormone." Ghrelin levels rise before meals, stimulating appetite and food-seeking behaviour. After eating, ghrelin levels decrease. Ghrelin also influences metabolic rate and fat storage. Chronic inadequate sleep and stress can dysregulate ghrelin signalling, increasing appetite independent of energy needs. Individual variation in ghrelin response is substantial.

Peptide YY (PYY) and Cholecystokinin (CCK)

Peptide YY is released by the intestines after food consumption, particularly in response to fat and protein. It signals fullness and reduces further eating. Cholecystokinin is released when dietary fat and protein are detected in the small intestine, promoting satiety and slowing gastric emptying. Both hormones work synergistically to promote postprandial satiety.

Glucagon-Like Peptide-1 (GLP-1)

GLP-1 is released by intestinal cells in response to nutrient intake, particularly glucose. It regulates blood glucose, promotes satiety, and slows gastric emptying. GLP-1 also affects glucose production in the liver. Individual variation in GLP-1 response to foods is significant and influences how different people respond to the same nutritional intake.

Insulin

Insulin is released in response to elevated blood glucose and amino acid levels. In addition to regulating glucose metabolism, insulin signals energy abundance to the brain and contributes to satiety. Chronic elevated insulin levels, as seen in insulin resistance, can interfere with appropriate appetite signalling despite adequate or excessive energy stores.

Mechanical and Neurological Factors

Beyond hormones, physical stomach and intestinal distension signals fullness mechanically. The vagus nerve transmits signals from the digestive tract to the brain. Gut microbiota also influence appetite through metabolite production and immune signalling. Sensory aspects of eating—flavour, aroma, and visual appearance—influence satiety independent of nutrient content.

Factors Affecting Satiety Signalling

Sleep quality and duration substantially influence satiety hormones. Inadequate sleep increases ghrelin and decreases leptin sensitivity, promoting increased appetite. Stress and elevated cortisol can dysregulate appetite signalling. Physical activity influences multiple satiety hormones. Meal composition (protein, fibre, and fat content) influences both the magnitude and duration of satiety signals. Individual genetic variation in satiety hormone receptors explains why people respond differently to the same foods.

Important Context