Satiety vs Satiation
Satiation is the set of signals that ends a meal in progress, while satiety is the post-meal inhibition that determines how long it takes before eating begins again.
Satiation and satiety describe two different windows. Satiation operates within a meal and terminates it, driven largely by gastric distension signalled through vagal afferents and by rapidly released gut peptides including cholecystokinin. Satiety is the between-meal state that suppresses the next eating occasion, sustained by GLP-1, peptide YY and amylin, and by the fall in ghrelin that follows nutrient arrival in the gut. Both converge on hindbrain and hypothalamic circuits, but they are dissociable and drugs act on them unequally.
GLP-1 receptor agonists work through both routes. Slowed gastric emptying enlarges the satiation signal for a given meal, but attenuates with continued exposure to long-acting agents, while central appetite suppression persists. Amylin analogues such as cagrilintide lean more heavily on satiation. In ad libitum test-meal studies they cut energy intake substantially at a sitting, and trials track the subjective side with visual analogue scales for hunger, fullness and prospective consumption.
Separating the two makes sense of a common report: early satiety, where a small volume of food feels intolerable, is a gastric phenomenon that tracks with nausea and often eases over weeks, while reduced hunger between meals persists and drives weight change. A patient describing one is not describing the other.
The vocabulary is used loosely, with satiety applied to any appetite reduction whatever the mechanism. Appetite ratings are self-reported and effectively impossible to blind when a drug causes nausea, so scale differences carry weak evidential weight on their own. And supplements advertised as boosting satiety hormones typically cite a small postprandial rise in endogenous GLP-1, orders of magnitude short of the exposure a receptor agonist produces.