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Dietary fiber-mediated mechanisms in carcinogenesis.
Cancer Res. 1992 Apr 01; 52(7 Suppl):2055s-2059s.CR

Abstract

Dietary fiber may affect the development of cancers of the gastrointestinal tract and the breast. The biological intermediates studied most have been fecal bile acids; both human and animal studies suggest a tumor-promoting role of bile acids in the development of colon tumors, although there are conflicting data from human studies. Short-chain fatty acids are major fermentation products of bacterial degradation of dietary fiber. If short-chain fatty acids explained the tumor-inhibiting properties of dietary fiber, the readily fermentable fibers such as guar and pectin would be more protective than cellulose and wheat bran, which has not been observed. Because these two hypotheses do not adequately explain modulation of tumor growth by dietary fiber, investigation of other intermediates is indicated. These include physical characteristics of the feces, such as abrasiveness; intestinal microflora; aqueous-phase bile acids, which may represent the bioavailable pool; alterations in mucins; mutagenicity of intestinal contents; alterations in mucosal cytokinetics; activities of enzymes, such as ornithine decarboxylase or aryl hydrocarbon hydroxylase; neurogenic effects caused by changes in intestinal bulk or short-chain fatty acids; gut hormones or other peptide growth factors (local or systemic); enterohepatic circulation of hormones; transit time; pH; or decreased availability of total dietary energy.

Authors+Show Affiliations

Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104.

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

1311988

Citation

Klurfeld, D M.. "Dietary Fiber-mediated Mechanisms in Carcinogenesis." Cancer Research, vol. 52, no. 7 Suppl, 1992, 2055s-2059s.
Klurfeld DM. Dietary fiber-mediated mechanisms in carcinogenesis. Cancer Res. 1992;52(7 Suppl):2055s-2059s.
Klurfeld, D. M. (1992). Dietary fiber-mediated mechanisms in carcinogenesis. Cancer Research, 52(7 Suppl), 2055s-2059s.
Klurfeld DM. Dietary Fiber-mediated Mechanisms in Carcinogenesis. Cancer Res. 1992 Apr 1;52(7 Suppl):2055s-2059s. PubMed PMID: 1311988.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary fiber-mediated mechanisms in carcinogenesis. A1 - Klurfeld,D M, PY - 1992/4/1/pubmed PY - 1992/4/1/medline PY - 1992/4/1/entrez SP - 2055s EP - 2059s JF - Cancer research JO - Cancer Res VL - 52 IS - 7 Suppl N2 - Dietary fiber may affect the development of cancers of the gastrointestinal tract and the breast. The biological intermediates studied most have been fecal bile acids; both human and animal studies suggest a tumor-promoting role of bile acids in the development of colon tumors, although there are conflicting data from human studies. Short-chain fatty acids are major fermentation products of bacterial degradation of dietary fiber. If short-chain fatty acids explained the tumor-inhibiting properties of dietary fiber, the readily fermentable fibers such as guar and pectin would be more protective than cellulose and wheat bran, which has not been observed. Because these two hypotheses do not adequately explain modulation of tumor growth by dietary fiber, investigation of other intermediates is indicated. These include physical characteristics of the feces, such as abrasiveness; intestinal microflora; aqueous-phase bile acids, which may represent the bioavailable pool; alterations in mucins; mutagenicity of intestinal contents; alterations in mucosal cytokinetics; activities of enzymes, such as ornithine decarboxylase or aryl hydrocarbon hydroxylase; neurogenic effects caused by changes in intestinal bulk or short-chain fatty acids; gut hormones or other peptide growth factors (local or systemic); enterohepatic circulation of hormones; transit time; pH; or decreased availability of total dietary energy. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/1311988/Dietary_fiber_mediated_mechanisms_in_carcinogenesis_ DB - PRIME DP - Unbound Medicine ER -