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The Effect of Dietary Polyunsaturated Acid (PUFA) Concentration and n6:n3 Ratio on Azoxymethane + Dextran Sodium Sulfate (AOM+DSS) Inflammation‐Associated Colorectal Cancer (CRC)
Author(s) -
Hintze Korry,
Kellen Sara,
Larson Deanna,
Ward Robert,
Lefevre Michael,
Hergert Nancie,
Benninghoff Abby
Publication year - 2015
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.29.1_supplement.753.6
Subject(s) - azoxymethane , polyunsaturated fatty acid , colorectal cancer , inflammation , carcinogenesis , linoleic acid , medicine , chemistry , endocrinology , food science , fatty acid , cancer , biochemistry
Previously, we showed that both the total dietary PUFA concentration and the ratio of n3 and n6 PUFA affected systemic inflammation when mice were challenged with lipopolysaccharide. Therefore, we sought to determine whether total PUFA concentration and/or ratio of n3 and n6 PUFA modulates CRC susceptibility using the AOM+DSS inflammation mediated model of colon cancer. Mice were fed the following diets that were identical except for the fat profile: 1) AIN93G control diet; 2) 10% (kcal) dietary PUFA, 1:1 n6:n3 ratio; 3) 10% PUFA, 20:1 n6:n3; 4) 2.5% PUFA, 1:1 n6:n3; or 5) 2.5% PUFA, 20:1 n6:n3. Dietary PUFA was provided as either linoleic or linolenic acid. Mice fed the AIN93G and the 2.5% PUFA, 1:1 n6:n3 diets had significantly higher colon tumor multiplicity than all other treatments ( P < 0.05). The n6:n3 ratio but not PUFA concentration had a significant effect on tumor size. Mice fed diets with a n6:n3 ratio of 1:1 had significantly larger tumors than mice fed the 20:1 n6:n3 ratio diets ( P = 0.012). Colon length was used to assess inflammation severity; however, there were no significant differences between treatments. These results suggest that the dietary PUFA profile may affect colorectal carcinogenesis and that higher ratios of n6 to n3 may be protective against AOM+DSS induced tumorigenesis. Support was provided by the Utah State University Office of Research and Graduate Studies.