What is the Origin of Central Satiety Signaling?

This term originates from neuroendocrinology and metabolic research, where "central" specifies the brain's role as the primary control center, and "satiety signaling" describes the biological communication related to the cessation of eating. Key discoveries of gut-derived hormones like leptin and ghrelin, and their actions on hypothalamic nuclei, solidified this concept as a major target for weight and metabolic health management.

What is the Mechanism of Central Satiety Signaling?

The mechanism centers on the arcuate nucleus of the hypothalamus, where peripheral signals such as insulin, leptin from fat cells, and PYY and GLP-1 from the gut converge. These hormones modulate the activity of two opposing neuronal populations: the anorexigenic pro-opiomelanocortin (POMC) neurons that promote satiety, and the orexigenic neuropeptide Y (NPY)/Agouti-related peptide (AgRP) neurons that stimulate appetite. A robust, responsive central satiety signaling system ensures appropriate caloric intake matching energy expenditure.

Central Satiety Signaling ∞ Area

Central Satiety Signaling

Meaning

Central satiety signaling refers to the complex neuroendocrine communication network within the brain, primarily involving the hypothalamus, that regulates the feeling of fullness and inhibits further food intake. This system integrates hormonal and neural signals from the gastrointestinal tract and adipose tissue to maintain energy balance and body weight homeostasis. Dysfunction in this intricate signaling process is a key driver of appetite dysregulation and metabolic imbalance.