ABSTRACT
Satiety, or the perception of fullness is the result of myriad sensory inputs ranging from allesthesia due to firing of interoceptive muscle stretch receptors on the stomach wall to cerebral glucostat receptors. Also contributing to satiety are visual and chemosensory influences. The search for the mechanism of satiety, not unlike Indiana Jones’ search for the Holy Grail, has been punctuated with twists and turns into the minutia of sensory system physiology and behavior. To undergrope this fully, let’s review this from a historical perspective. Anecdotally and through personal experience, it has been dogma that hunger originated from signals from the stomach. Institutively, this is logical, since food deprivation induces hunger and “hunger pangs,” a vague sense of abdominal emptiness, as contrasted to the post-holiday gorging and abdominal and stomach distension and fullness experienced with overeating. Hence, the satiety center migrated from the stomach, rostrally to land in the skull—in particular, the ventromedial nucleus of the hypothalamus.
