Consumption of a Western Diet Enhanced Colitis-Associated Colorectal Cancer and Dysbiosis of the Fecal Microbiome in Mice Notwithstanding Dietary Intervention or Fecal Microbiome Transfer
Date of Award:
Doctor of Philosophy (PhD)
Animal, Dairy, and Veterinary Sciences
Abby D. Benninghoff
Abby D. Benninghoff
Korry J. Hintze
In a rodent model of inflammation-associated colorectal cancer, consumption of a Western-style diet increases gut inflammation and enhances risk of developing colon tumors. The goal of this dissertation was to understand the contribution of bacteria within the large intestine on colon inflammation and colon tumorigenesis. Two pre-clinical animal studies were performed using two different intervention strategies to shift the microbiome, and potentially gut inflammation and tumor development: 1) an experiment using dietary supplementation with black raspberries, a functional food enriched in bioactive anthocyanins with purported antiinflammatory activity, and 2) an experiment using fecal microbiota transfer from mice fed a healthy diet with low symptoms of colitis or mice fed a Western diet with severe symptoms of colitis to recipient mice fed either the healthy or Western diet directly. Dietary supplementation with black raspberries did reduce colon tumor number, irrespective of the basal diet, and caused significant shifts in the composition of the gut microbiome. Fecal microbiota transfer from mice with severe colitis did not exacerbate colitis in recipient mice fed a healthy diet, nor did transfer from mice with low symptoms protect mice fed a Western diet. However, for both experiments, we determined that the basal diet fed to the recipient mice was the driving factor affecting the gut inflammation and colon tumorigenesis.
Rodriguez Jimenez, Daphne Michelle, "Consumption of a Western Diet Enhanced Colitis-Associated Colorectal Cancer and Dysbiosis of the Fecal Microbiome in Mice Notwithstanding Dietary Intervention or Fecal Microbiome Transfer" (2023). All Graduate Theses and Dissertations. 8802.
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