Inhibition of gastric emptying by glucose depends on length of intestine exposed to nutrient

Abstract

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.

Leu72Met408 Polymorphism of the Ghrelin Gene Is Associated With Early Phase of Gastric Emptying in the Patients With Functional Dyspepsia in Japan

“…In addition, gastric emptying and duodenal glucose delivery are closely regulated. 42,43 Early phase of gastric emptying is usually 5-15 minutes in duration and is influenced by intragastric drink volume and associated with duodenal glucose delivery. 42,44,45 In this study, AUC 15 value as a marker of early phase of gastric emptying was significantly associated with the Leu72Met408 gene SNP in FD patients.…”

Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects

“…The presence of carbohydrate in the small intestine is a well established stimulus for GLP-1 and GIP secretion, leading to glucose-dependent insulin secretion from the ␤-cells and feedback that regulates gastric emptying (24). Direct exposure of carbohydrate to the mucosa of the small intestine appears to be an essential requirement for GLP-1 and GIP secretion (10), and the magnitude of the former is dependent on the rate of delivery of glucose into the small intestine (35).…”

Influences of fat restriction and lipase inhibition on gastric emptying in obesity

“…[45][46][47] The latter hypothesis required the measuring of fat in the stools which would have interfered with the double-blind set-up of the study. Therefore, we started with the first part of our hypothesis.…”