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AJP - Gastrointestinal and Liver Physiology, Vol 256, Issue 2 404-G411, Copyright © 1989 by American Physiological Society
ARTICLES |
H. C. Lin, J. E. Doty, T. J. Reedy and J. H. Meyer
Department of Medicine, Veterans Administration Medical Center, Sepulveda, California 91343.
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.
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