Lin H C, Doty J E, Reedy T J, Meyer J H
Department of Medicine, Veterans Administration Medical Center, Sepulveda, California 91343.
Am J Physiol. 1989 Feb;256(2 Pt 1):G404-11. doi: 10.1152/ajpgi.1989.256.2.G404.
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.
营养素以剂量相关的方式抑制胃排空。我们推测，负荷依赖性胃排空是由于黏膜吸收机制饱和所致，因此随着更多营养素进入肠道参与这种负反馈，更长的小肠段会暴露于未吸收的营养素中。为了验证这一观点，我们在17只狗身上将0.25至1.0M葡萄糖餐的暴露限制在十二指肠和空肠的不同长度。然后将这些有限灌注的效果与整个肠道（ALL）暴露于营养素的实验进行比较。1.0M餐出现最大抑制，150cm灌注和ALL灌注的情况相似。相比之下，即使是1.0M负荷，当葡萄糖餐局限于十二指肠近端的前15cm时，未观察到胃排空受到抑制。当1.0M餐局限于近端65cm时，仅观察到最大抑制的50 - 60%。我们得出结论，近端和远端肠道均存在葡萄糖感受器，且抑制作用与暴露于葡萄糖的小肠长度有关。
