Lin H C, Doty J E, Reedy T J, Meyer J H
Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048.
Am J Physiol. 1990 Dec;259(6 Pt 1):G1031-6. doi: 10.1152/ajpgi.1990.259.6.G1031.
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.
此前，我们报道过葡萄糖或酸对胃排空的抑制作用取决于肠道暴露于抑制剂的长度[《胃肠病学》95:A877，1988；《美国生理学杂志》256(胃肠肝脏生理学19):G404 - G411，1989]。在本研究中，我们假设脂肪的反馈控制可能受到类似的调节。在患有慢性肠瘘的狗中，我们比较了不同长度的小肠暴露于3、9或27 mM油酸钠餐时肠道反馈的强度。我们发现：1)液体排空的抑制呈剂量依赖性；2)负反馈的强度取决于油酸盐的浓度和暴露于脂肪的肠道长度；3)脂肪暴露于150 cm肠道时达到完全抑制效果；4)肠道远端一半的抑制作用不如近端一半产生的抑制作用强；5)以摩尔计，油酸盐抑制胃排空的效果是葡萄糖的20倍，这种差异与脂肪吸收速度较慢有关。
