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Effects of dietary resistant starch on beta‐catenin in azoxymethane‐treated colonic epithelium
Author(s) -
Cray Nicole,
Pillatzki Angela,
Zhao Yinsheng,
Birt Diane F,
Whitley Elizabeth M
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.874.9
Subject(s) - azoxymethane , wnt signaling pathway , aberrant crypt foci , laser capture microdissection , crypt , resistant starch , colorectal cancer , beta catenin , medicine , epithelium , 1,2 dimethylhydrazine , carcinogenesis , biology , endocrinology , cancer research , signal transduction , cancer , gene expression , pathology , biochemistry , starch , gene , colonic disease
Resistant starches (RS) have been suggested to reduce colon cancer through production of short chain fatty acids by microflora. Aberrant Wnt signaling is common in colorectal cancer, with mis‐regulation and over‐expression of beta‐catenin. We hypothesize that RS will modulate the Wnt pathway in colonic epithelial cells. We evaluated mRNA levels of beta‐catenin in colonic epithelial cells, comparing results from F344 rats fed for 8 weeks with diets containing Guat209 (Guat), AR16035 (AR), or a cross (ARxGuat), with 34.5% 1.2%, and 1.9% RS, respectively. Carcinogenesis was initiated by azoxymethane (AOM) before RS was fed. Populations of histologically normal epithelial cells of the mucosal surface and crypt base were collected by laser microdissection and quantative PCR performed for beta‐catenin. Preliminary results demonstrate no difference between beta‐catenin mRNA levels in colonic epithelium from non‐AOM‐treated rats fed low‐ or high‐RS diets, or associated with AOM‐treatment in rats fed low‐RS diets. Without AOM initiation, regardless of the diet, expression of beta‐catenin is similar in each niche. Dietary RS may provide a means to regulate Wnt signaling in the colon.