Stimulation of ammonia production from glutamine by intraluminal glucose in small intestine of dogs.

Previous studies have shown that the quantity of ammonia derived from the small intestinal metabolism of arterial glutamine was equal to ammonia released by the colon. Little is known, however, about processes that may alter small intestinal glutamine metabolism. The purpose of this study was to evaluate the effect of intraluminal, nonnitrogenous compounds on ammonia release into mesenteric venous blood and glutamine uptake from arterial blood by in situ intestinal segments in anesthetized, fasted dogs. In paired luminal perfusion studies, either 50 mM glucose, 3-O-methylglucose, or 3-hydroxybutyric acid was compared with a control perfusate containing 50 mM mannitol. In the jejunum, glucose perfusion significantly increased ammonia release into mesenteric venous blood by 21 +/- 5 nmol.min-1.g intestine-1 or 32 +/- 7% and glutamine uptake from arterial blood by 21 +/- 3 nmol.min-1.g intestine-1. Perfusion of ileum with glucose also significantly increased ammonia release by 8 +/- 1 nmol.min-1.g intestine-1 or 12 +/- 2% and glutamine uptake by 11 +/- 4 nmol.min-1.g intestine-1, although the increments were less than in the jejunum. Perfusion of the jejunum with 3-hydroxybutyric acid or nonmetabolizable 3-O-methylglucose caused no increase in ammonia release, even though glucose, 3-hydroxybutyric acid, and 3-O-methylglucose were absorbed at similar rates and there were similar increments in water absorption. The results indicated that glucose absorbed from the lumen of both the jejunum and ileum stimulated glutamine uptake from arterial blood and ammonia release into mesenteric venous blood. These effects were quantitatively greater in the jejunum. Stimulation of intestinal glutamine metabolism was probably related to cellular metabolism of glucose and could not be attributed to a stimulation of solute or water absorption.