Dynamics of feeding behavior: role of hypothalamic and satiety signals

Abstract

How are rats, people, and many other omnivores able to regulate food intake both within a meal and over days and weeks? We introduce a homeostatic computational theory for eating regulation whose components can be readily interpreted in terms of neuronal circuits. We propose that the long-term set point (over months and years) is located in the hypothalamus and is modulated both by signals for adiposity as well as some signals from the gut, and also by psychological factors such as learning and arousal (emotion). Hypothalamic efferents are inputs to the hindbrain (principally the nucleus tractus solitarius: NTS) providing the set point for short-term eating regulation. Satiety signals (SSs) and delayed gustatory and gastrointestinal aftereffects of eating act via the NTS as neural feedback governing short-term regulation (within a meal or a day). The model hypothesizes that the NTS acts as a comparator in a feedback control system. When the delayed sequelae of eating (SSs) fall below the short-term set point, eating begins, in on–off fashion. The ingestion of food increments the SSs after a delay; the increasing SSs eventually turn eating off. The model forges real links between a functioning feedback mechanism, neuro–hormonal data, and both short-term (meals) and long-term (eating-rate regulation) behavioral data. The model can explain relevant data from behavioral experiments and has implications for diet and nutrition.