pectins and Intestinal-Neoplasms

The influence of various dietary supplements on the fecal bacteria was studied. Substances were chosen for study because they were known to influence body metabolism or had been implicated in the various hypotheses as the cause of large bowel cancer. No alteration in the fecal flora was demonstrated. The implications of these findings are discussed in the light of other investigations with special reference to our theory concerning the cause of large bowel cancer.

Topics: Adult; Bacteria; Cholesterol; Diet; Dietary Fats; Dietary Fiber; Feces; Fruit; Humans; Intestinal Neoplasms; Male; Pectins; Triglycerides

APC-germline mutation creates predisposition for intestinal tumorigenesis. APCMin/+ mice, developing tumors preferentially in the small intestine and only minimally in the colon, were fed pectin-enriched diets (10% galacturonan; degree of methoxylation=37.0 and 70.4%) or standard diet. Pectins used in the present study do not inhibit intestinal tumorigenesis and rather accelerate it in APCMin/+ mice. Both pectins exhibited prebiotic effects associated with high fermentative formation of acetate but producing low butyrate. The differences of the short-chain fatty acid concentrations between cecum and colon and those between colon and feces were larger than expected and increased with cancer progression, indicating an inhibition of butyrate absorption. Pectins transported more bile acids toward the colon than the standard diet and caused a higher generation of secondary bile acids despite lower pH values. Overexpression of COX-2 resulted in lower antioxidative capacity, thus promoting cancer. Apoptosis increased in hyperplasia but decreased in late adenomas. When biological modular design principles are taken into consideration, it can be expected that pectin also reinforces colorectal tumorigenesis of patients suffering from APC gene defects.

Topics: Acetates; Animals; Antineoplastic Agents; Butyrates; Cyclooxygenase 2; Fatty Acids, Volatile; Female; Fermentation; Genes, APC; Germ-Line Mutation; Immunohistochemistry; Intestinal Absorption; Intestinal Mucosa; Intestinal Neoplasms; Mice; Mice, Inbred BALB C; Pectins