Dietary resistant starch and chronic inflammatory bowel diseases

Citation
G. Jacobasch et al., Dietary resistant starch and chronic inflammatory bowel diseases, INT J COL R, 14(4-5), 1999, pp. 201-211
Citations number
50
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
ISSN journal
01791958 → ACNP
Volume
14
Issue
4-5
Year of publication
1999
Pages
201 - 211
Database
ISI
SICI code
0179-1958(199911)14:4-5<201:DRSACI>2.0.ZU;2-O
Abstract
These studies were performed to test the benefit of resistant starch on ulc erative colitis via prebiotic and butyrate effects. Butyrate, propionate, a nd acetate are produced in the colon of mammals as a result of microbial fe rmentation 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, an d DNA content of the colonocytes. They also ameliorate symptoms of ulcerati ve colitis in human patients and rats injected with trinitrobenzene sulfoni c acid (TNBS). Butyrate, and also to a lesser degree propionate, are substr ates for the aerobic energy metabolism, and trophic factors of the colonocy tes. Adverse butyrate effects occur in normal and neoplastic colonic cells. In normal cells, butyrate induces proliferation at the crypt base, while i nhibiting 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 e arlier in the resistant starch (RS)-fed rats than in the RS-free group. Thi s benefit coincided with activation of colonic epithelial cell proliferatio n and the subsequent restoration of apoptosis. The noncollagenous basement membrane protein laminin was regenerated initially in the RS-fed group, dem onstrating what could be a considered lower damage to the intestinal barrie r function. The calculation of intestinal short-chain fatty acid absorption confirmed this conclusion. The uptake of short-chain fatty acids in the co lon is strongly inhibited in the RS-free group, but only slightly reduced i n the animals fed with RS. Additionally, RS enhanced the growth of intestin al bacteria assumed to promote health. Further studies involving patients s uffering 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.