Satiety Hormones Explained

The Satiety System

While ghrelin signals hunger, multiple hormones work together to communicate satiety—the state of having consumed adequate food. These satiety signals reduce the motivation to eat and promote the sensation of fullness. Understanding this system is essential for comprehending how the body regulates food intake.

Satiety is not instantaneous. It develops over time through multiple signals: oral sensations from eating, gastric stretch from a full stomach, nutrient absorption, and hormonal cascades triggered by food consumption. This multi-system approach creates redundancy, ensuring that the body receives consistent signals about nutritional status.

Leptin: The Long-Term Energy Regulator

Leptin is a hormone produced by adipose (fat) tissue that signals the brain about long-term energy stores. When fat stores are adequate, leptin levels rise, signaling the brain that sufficient energy is available. This signal reduces appetite and increases energy expenditure. Conversely, when fat stores decline, leptin levels drop, increasing hunger.

However, leptin's function is more complex than a simple on-off switch. The brain's sensitivity to leptin varies among individuals and changes under different conditions. A state called leptin resistance can develop in some individuals, where despite high leptin levels, the brain does not respond appropriately to the satiety signal. This condition is associated with obesity and altered appetite regulation.

Factors Influencing Leptin:

• Body fat percentage and distribution
• Caloric intake and fasting duration
• Sleep quality and circadian rhythms
• Inflammatory markers and oxidative stress
• Insulin sensitivity and glucose metabolism
• Age and hormonal status

Peptide YY: Meal-Related Satiety Signal

Peptide YY (PYY) is released from intestinal cells in response to food consumption, particularly fat and protein. PYY levels rise after eating and contribute to short-term satiety—the feeling of fullness during and after a meal. This hormone acts on the brain to reduce hunger and food intake.

GLP-1: The Multifunctional Satiety Hormone

Glucagon-like peptide 1 (GLP-1) is released from intestinal cells in response to glucose and other nutrients. This hormone has multiple roles in regulating food intake and metabolism:

• Appetite Suppression: GLP-1 acts on brain centers to reduce appetite and promote satiety.
• Gastric Emptying: GLP-1 slows the rate at which the stomach empties, prolonging the sensation of fullness.
• Insulin Secretion: GLP-1 stimulates insulin release in response to rising blood glucose, supporting nutrient uptake.
• Glucose Regulation: GLP-1 helps maintain stable blood glucose levels after meal consumption.

Individual variation in GLP-1 responsiveness affects how quickly satiety develops and how long it persists. Some individuals experience more robust GLP-1 responses to meals, contributing to stronger satiety signals and potentially lower overall food intake.

Other Satiety Signals

Cholecystokinin (CCK)

Released by the small intestine in response to dietary fat and protein, CCK promotes fullness and reduces meal size. This hormone also stimulates gallbladder contraction to aid fat digestion.

Gastric Stretch

Mechanical stretch of the stomach activates nerve signals to the brain, contributing to fullness even before nutrient absorption occurs. This signal is why meal volume affects satiety independently of caloric content.

Nutrient Sensing

Specialized cells in the intestine and liver sense the presence and concentration of glucose, amino acids, and fatty acids. These signals contribute to satiety through multiple pathways, not all fully understood.

Vagal Signaling

The vagus nerve transmits signals from the gastrointestinal tract to the brain, communicating information about meal composition, distension, and nutrient absorption.

Individual Variation in Satiety Response

While satiety hormones follow general patterns, individual responses vary considerably. Some people experience robust, prolonged satiety signals and feel full for extended periods after eating. Others experience weaker satiety responses, leading to faster hunger return and increased food consumption.

Sources of this variation include:

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