Disaccharidase Activity in Rat Cecum and Colon with Hyperplasia Induced by Maltitol or Glucomannan

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概要

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• The existence of disaccharidases and an enzyme that hy-drolyzes maltitol were investigated in the large intestine of rats. In ad-dition, the properties of disaccharidases were studied in the cecum and colon with hyperplasia induced by the ingestion of nondigestible car-bohydrates such as maltitol and glucomannan. Maltase activity was de-tected in the cecal and colonic mucosa of rats fed a regular diet, although it was a very low level as compared with that in the small intestinal mucosa. Maltitol hydrolysis was notably lower in the cecum and colon than in the small intestine. The Km of maltose was 5.56mM in the small intestine and 5.59mM in the cecum, while that in the colon was 2.56mM. The Vmax of maltose was at very low levels in the cecum (0.38μmol/mg protein/h) and colon (0.37μmol/mg protein/h) in comparison with that in the small in-testine (30.3μmol/mg protein/h). With regard to the maltitol hydrolyzing enzyme, Km and Vmax were 2.00 mM and 2.51μmol/mg protein/h in the small intestine, respectively. Km and Vmax in the cecum and colon could not be measured because the level was too low. The tissue weights of the cecum and colon increased significantly in both the maltitol (p<0.01, p<0.05) and glucomannan (p<0.01, p<0.05) groups in comparison with that of the control group. The specific activity of maltase decreased significantly in the small intestine of the maltitol (p<0.05) and glu-comannan (p<0.01) groups. However, maltase activity in the cecum and colon was not lowered by maltitol ingestion, although it decreased significantly in the cecum of the glucomannan group (p<0.01). Sucrase activity in the small intestine and cecum was decreased significantly by maltitol (p<0.05, p<0.01) or glucomannan (p<0.01, p<0.01) ingestion, whereas it was not decreased in the colon. Maltitol hydrolyzing activity did not decrease significantly in the small intestine of the maltitol group, although that in the cecum and colon was not measured exactly by the methods used here. These results demonstrate that disaccharidases exist in the cecal and colonic mucosa of rat, and that they are not induced even in the tissue with hyperplasia, which is caused by maltitol ingestion.

• 財団法人 学会誌刊行センターの論文

著者

• OKU Tsuneyuki

  Department of Nutrition, Faculty of Medicine, The University of Tokyo

• KWON Sunja

  Department of Nutrition, School of Health Sciences, Faculty of Medicine

• OKU Tsuneyuki

  Department of Nutrition, School of Health Sciences, Faculty of Medicine

関連論文

• Transitory Laxative Threshold of Trehalose and Lactulose in Healthy Women
• Disaccharidase Activity in Rat Cecum and Colon with Hyperplasia Induced by Maltitol or Glucomannan
• Development of 1,25-dihydroxycholecalciferol receptor in the duodenal cytosol of chick embryo.
• Metabolic Fate of Ingested (14C)-Maltitol in Man.

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