Gastrointestinal satiety in animals other than man

The present paper reviews the development of some of our ideas of how physiological stimuli on the gastrointestinal tract contribute to the onset of satiety.The various signals originating from the gut caused by stretch, osmo-concentration or specific chemical stimuli must be relayed to the brain, either neurally or hormonally, to be integrated with post-absorptive signals from other sites including the brain itself.to produce a response, which will also take into account the animal's previous experience.the importance of the different signals varying with the feeding regimen.In free-feeding animals, individual meal size varies and relatcs to the succeeding inter-meal interval (Le Magnen, 1983).so that long-term intake can be adjusted by the number of meals.In animals that are meal-fed once or twice daily, long-term intake relates to meal size, which must involve a learned anticipation of metabolic requirements.As the meal terminates long before absorption is complete, meal size will be largely signalled from the gastrointestinal tract. PREGASTRIC FOOD STIMULI ALONE CANNOT CONTROL. MEAL S I Z EIn free-feeding sham-fed rats, in which stomach contents are allowed to drain o u t continuously.feeding was prolonged in the first meal after opening the cannula (Davis & Campbell, 1973), showing that feedback signals from the stomach and small intestine must normally initiate satiety.The gastrointestinal signalling of meal size is not, therefore.an unconditioned stimulus for the learned oral control of intake from the texture and taste of food.S T O M A C H CONTROL O F INTAKE Gastric distension (e.g.placing inert gum or a balloon in the stomach of the dog through a gastric fistula; see Janowitz & Grossman, 1949) has long been known to decrease food intake.In the rat, the stomach can sense both the amount and composition of the food when onward passage of digesta is prcvented by a pyloric noose, even after vagotomy (Kraly & Gibbs, 1980).The existence of a stomach satiety factor has been suggested as food placed in extra transplanted (and hencc decentralized) stomachs in inbred Lewis rats reduced intake by mouth in a dose-related manner (Koopmans, 1983).