The site of the interaction between dietary fiber and the small intestine and its nutritional significance in rats fed excessive doses of Food Red No. 2.

在不同消化道切除大鼠中，研究了膳食纤维（DF）对食物红2号（苋菜，Am）中毒剂量大鼠的摄食量、生长率、摄食效率以及日粮蛋白质消化率和生物学价值的影响机制。体重约100 g的大鼠行空肠切除术、回肠切除术、空肠-回肠切除术（剩余约10%小肠）、盲肠切除术（带或不带回盲瓣）、回肠-直肠吻合术。生长恢复后，分别饲喂纯化基础饲粮(B)、B + 5% Am (C)和C + 5% DF (BDF) 3种饲粮。结果表明：(1)与去空肠大鼠相比，在B粮中添加5% Am对去回肠大鼠生长速度的抑制更为严重，说明空肠是Am毒性发生的主要部位。(2)在去空肠和回肠大鼠的日粮C中同时添加5% BDF，完全消除了am毒性，说明BDF在小肠管腔中发挥了有益作用。Am和BDF的这些作用与饲粮蛋白质源的消化吸收效率相一致。BDF的作用必须在小肠剩余长度至少达到50%时才会出现。当剩余小肠长度达到10%时，BDF的作用消失。因此，为了发挥BDF的作用，需要一定长度的小肠来充分相互作用。(3)我们发现BDF的有益作用是由于延缓了食糜的小肠转运速度（SITS）。延迟sit可促进饲粮中Am抑制的营养物质的利用。(4)此外，sit的延迟被认为是由于小肠黏膜内源性阿片类药物释放增强引起的，因为50 ppm的膳食盐酸吗啡部分保护了am毒性。

The mechanism(s) by which dietary fiber (DF) exerts beneficial effects on food intake, growth rate, food efficiency, and digestibility and biological value of dietary protein in rats fed toxic dosed of Food Red No. 2 (amaranth, Am) were investigated in rats received resection at different sites of digestive tract.Jejunectomy, ileectomy, jejuno-ileal resection (remaining about 10% of the small intestine), cecectomy (with or without ileocecal valve), and ileo-rectostomy were performed in rats weighing about 100 g. After growth recovery, they were fed 3 types of diets: purified basal diet (B), B plus 5% Am (C), and C plus 5% DF (prepared from sugar beet, BDF).The results obtained were as follows:(1) The growth rate of ileectomized rats were more severely depressed by the addition of 5% Am to the diet B compared with that of jejunectomized rats: the results show that the jejunum is the main site of development of Am-toxicity.(2) The concurrent addition of 5% BDF to diet C completely eliminated Am-toxicity in both Jejunectomized and ileectomized rats, showing that beneficial effects of BDF is realized in the lumen of the small intestine. These effects of Am and BDF were compatible with the digestive-absorptive efficiency for dietary protein source. BDF's effects necessarily developed when the remaining small intestinal length was at least 50%. When the remaining small intestine was 10% of the entire length, BDF's effect disappeared. Therefore for the development of BDF's effect, a certain length of the small intestine is required to sufficiently interact each other.(3) We found that beneficial effects of BDF was due to dlaying the small intestinal transit speed (SITS) of the chyme. Delay of SITS enhanced the utilization of nutrients which were inhibited by dietary Am.(4) Moreover, delay of SITS was considered to be caused by enhanced release of endogeneous opioids from small intestinal mucosa, since 50 ppm dietary morphine hydrochloride partially protected Am-toxicity.