Dietary resistant starch and chronic inflammatory bowel diseases
| Autor: | Gisela Jacobasch, D. Schmiedl, K. Schmehl, Martin Kruschewski |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
food.ingredient Colon Crypt Inflammation Apoptosis Butyrate Biology Rats Sprague-Dawley food Internal medicine medicine Dietary Carbohydrates Animals Humans Resistant starch chemistry.chemical_classification Cell growth Gastroenterology Fatty acid Starch medicine.disease Fatty Acids Volatile Inflammatory Bowel Diseases Ulcerative colitis digestive system diseases Rats Butyrates Endocrinology chemistry Biochemistry Intestinal Absorption Trinitrobenzenesulfonic Acid Bacterial Translocation medicine.symptom |
| Zdroj: | International journal of colorectal disease. 14(4-5) |
| ISSN: | 0179-1958 |
| Popis: | These studies were performed to test the benefit of resistant starch on ulcerative colitis via prebiotic and butyrate effects. Butyrate, propionate, and acetate are produced in the colon of mammals as a result of microbial fermentation of resistant starch and other dietary fibers. Butyrate plays an important role in the colonic mucosal growth and epithelial proliferation. A reduction in the colonic butyrate level induces chronic mucosal atrophy. Short-chain fatty acid enemas increase mucosal generation, crypt length, and DNA content of the colonocytes. They also ameliorate symptoms of ulcerative colitis in human patients and rats injected with trinitrobenzene sulfonic acid (TNBS). Butyrate, and also to a lesser degree propionate, are substrates for the aerobic energy metabolism, and trophic factors of the colonocytes. Adverse butyrate effects occur in normal and neoplastic colonic cells. In normal cells, butyrate induces proliferation at the crypt base, while inhibiting proliferation at the crypt surface. In neoplastic cells, butyrate inhibits DNA synthesis and arrests cell growth in the G1 phase of the cell cycle. The improvement of the TNBS-induced colonic inflammation occurred earlier in the resistant starch (RS)-fed rats than in the RS-free group. This benefit coincided with activation of colonic epithelial cell proliferation and the subsequent restoration of apoptosis. The noncollagenous basement membrane protein laminin was regenerated initially in the RS-fed group, demonstrating what could be a considered lower damage to the intestinal barrier function. The calculation of intestinal short-chain fatty acid absorption confirmed this conclusion. The uptake of short-chain fatty acids in the colon is strongly inhibited in the RS-free group, but only slightly reduced in the animals fed with RS. Additionally, RS enhanced the growth of intestinal bacteria assumed to promote health. Further studies involving patients suffering from ulcerative colitis are necessary to determine the importance of RS in the therapy of a number of intestinal diseases and the maintenance of health. |
| Databáze: | OpenAIRE |
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