Nutrients inhibit gastric emptying in a dose-related fashion. We postulated that load-dependent gastric emptying results from the saturation of mucosal absorptive mechanisms, so that a longer length of the small intestine is exposed to unabsorbed nutrients as more nutrient enters the intestine to participate in this negative feedback. To test this idea, we limited exposure of 0.25 to 1.0 M glucose meals to various lengths of duodenum and jejunum in 17 dogs. The effects of these limited perfusions were then compared with experiments in which the whole gut (ALL) was exposed to the nutrient. Maximal inhibition was seen with 1.0 M meal and was similar with perfusions of 150 cm and ALL. By contrast, even with the 1.0 M load, no inhibition of gastric emptying was seen when glucose meal was confined to the first 15 cm of the proximal duodenum. Only 50-60% of maximal inhibition was observed during confinement of 1.0 M meal to the proximal 65 cm. We concluded that glucose sensors are present in both the proximal and the distal gut and the inhibition was related to the length of the small intestine exposed to glucose.

Previously, we reported that inhibition of gastric emptying by glucose or acids depends on the length of gut exposed to the inhibitor [Gastroenterology 95: A877, 1988; Am. J. Physiol. 256 (Gastrointest. Liver Physiol. 19): G404-G411, 1989]. In this study, we hypothesized that feedback control by fat may be similarly regulated. In dogs with chronic intestinal fistulas, we compared the intensity of intestinal feedback when different lengths of the small intestine were exposed to meals of 3, 9, or 27 mM sodium oleate. We found that 1) inhibition of liquid emptying was dose dependent, 2) intensity of negative feedback was dependent on both the concentration of the oleate and the length of gut exposed to fat, 3) full inhibitory effect was achieved with exposure of fat to 150 cm of gut, 4) inhibition from the distal one-half of gut was less potent than that generated from the proximal one-half of gut, and 5) on a molar basis oleate was 20 times as effective as glucose at inhibition of gastric emptying and that this difference was related to the slower rate of fat absorption.

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Exposure of the small intestine to acid inhibits gastric emptying in a dose-related fashion that depends on titratable acidity and pH. Little information is available on the location of this inhibitory mechanism or on the relative contribution of titratable acidity and pH to this feedback control. We hypothesized that the dependence on titratable acidity is related to the length of the intestine exposed to acid and that the dependence on pH is related to the region of the intestine exposed to acid. To test these ideas, we studied 11 dogs with duodenal and jejunal fistulas. The inhibitory effects were tested when different lengths of the small intestine were exposed to test solutions of 0.03, 0.06, and 0.12 meq/ml titratable acidities. pH as an independent covariable was separated from titratable acidity by comparing the inhibition of gastric emptying of lactic acid (pH fixed to 2.4) to HCl (pH 0.96-1.6). Maximal inhibition of gastric emptying by both acids depended on acid exposure of a length of small intestine that was greater than 65 but less than or equal to 150 cm long. When acid was confined to the proximal 15 cm, increasing concentration of HCl (decreasing pH) resulted in increasing inhibition, but this effect was absent with increasing concentration of lactic acid (fixed pH). Inhibition was absent when 0.06 meq/ml HCl was infused into the intestine beyond the midintestine.(ABSTRACT TRUNCATED AT 250 WORDS)