A number of ways in which the intestine might participate in the induction of satiety have been examined using direct intestinal injections to alter the contents of the duodenum and then observing the effect on subsequent food intake over a 2K-hr period. The injection of either bulk or hypertonic solutions (NaCl or glucose) into the duodenum suppressed food intake. The injection of substantial amounts of food did not have an effect greater than that caused by equivalent amounts of nonnutritive bulk and the injection of acid material did not suppress eating more than basic material. These results suggest that bulk and osmotic pressure in the duodenum may initiate physiological changes which can ultimately participate in the regulation of meal size but that metabolites, duodenal hormones, and specific dynamic action do not. With the gastrointestinal system intact, the flow of material from the stomach to the intestine would be sufficiently slow that neither changes in duodenal bulk nor osmotic pressure would be involved in the regulation of meal size. When the stomach is partially removed or denervated, the rate of passage of food into the duodenum may increase enough so that osmotic and bulk signals originating in the duodenum would help to regulate meal size.
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