Dietary resistant starch and chronic inflammatory bowel diseases (original) (raw)

Abstract

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.

Access this article

Log in via an institution

Subscribe and save

Buy Now

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

Author information

Authors and Affiliations

  1. Department of Food Chemistry and Preventive Nutrition, German Institute of Human Nutrition Potsdam-Rehbrücke, Arthur-Scheunert-Allee 114–116, D-14558 Bergholz-Rehbrücke, Germany e-mail: jaco@www.dife.de, Tel.: +49-33200-88543, Fax: +49-33200-88280, , , , , , DE
    G. Jacobasch, D. Schmiedl & K. Schmehl
  2. Surgical Clinic I, General, Thoracic, and Vascular Surgery, Benjamin Franklin Medical Center, Free University of Berlin, Berlin, Germany, , , , , , DE
    M. Kruschewski

Authors

  1. G. Jacobasch
    You can also search for this author inPubMed Google Scholar
  2. D. Schmiedl
    You can also search for this author inPubMed Google Scholar
  3. M. Kruschewski
    You can also search for this author inPubMed Google Scholar
  4. K. Schmehl
    You can also search for this author inPubMed Google Scholar

Additional information

Accepted: 11 August 1999

Rights and permissions

About this article

Cite this article

Jacobasch, G., Schmiedl, D., Kruschewski, M. et al. Dietary resistant starch and chronic inflammatory bowel diseases.Int J Colorect Dis 14, 201–211 (1999). https://doi.org/10.1007/s003840050212

Download citation