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.

Research Project

Project/Area Number	59480054
Research Category	Grant-in-Aid for General Scientific Research (B)
Allocation Type	Single-year Grants
Research Field	応用生物化学・栄養化学
Research Institution	Hokkaido University
Principal Investigator	KIRIYAMA Shuhachi 北海道大学, 農学部, 教授 (00035396)
Co-Investigator(Kenkyū-buntansha)	知地英征北海道大学, 農学部, 助手 (20002066)
Project Period (FY)	1984 – 1985
Project Status	Completed (Fiscal Year 1985)
Budget Amount *help	¥7,200,000 (Direct Cost: ¥7,200,000) Fiscal Year 1985: ¥500,000 (Direct Cost: ¥500,000) Fiscal Year 1984: ¥6,700,000 (Direct Cost: ¥6,700,000)
Keywords	dietary fiber / amaranth toxicity / rat / small intestinal transit speed / 内因性オピオイド
Research Abstract	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.