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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #415342
Research Project: Modification of Diurnal Patterns to Promote Health in Models for Human Metabolic Dysfunction

Location: Dietary Prevention of Obesity-related Disease Research

Title: Oncogenic signatures and inflammatory colon in diet-induced obese mouse models

Author
item Zeng, Huawei

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 11/7/2024
Publication Date: 11/7/2024
Citation: Zeng, H. 2024. Oncogenic signatures and inflammatory colon in diet-induced obese mouse models. International Conference on Innovations and Advances In Cancer Research and Treatment, November 6-7, 2024 Boston, MA. abstract.

Interpretive Summary:

Technical Abstract: Adoption of an obesogenic diet such as a high-fat diet (HFD) results in obesity, bacterial dysbiosis, chronic inflammation, and cancer. Primary bile acids (BAs) play critical roles in cholesterol metabolism, lipid digestion, and host-microbe interaction. However, HFDs increase secondary BAs (e.g., deoxycholic acid (DCA) and lithocholic acid (LCA) in the colon), are risk factors for colonic inflammation and cancer. Gut bacteria and their metabolites are recognized by interleukin-1 (IL-1R)/toll-like receptors (TLRs) which are essential to maintain intestinal homeostasis; host extracellular microRNAs (miRNAs) can alter bacterial growth in the colon. Characterization of the underlying mechanisms may lead to identifying fecal oncogenic signatures reflecting colonic health. We hypothesize that a HFD accelerates the inflammatory process, oncogenic metabolites, and disease-related gut microbiome in the colon. With diet-induced obese mouse models, we found that the concentrations of plasma interleukin 6 (IL-6), inflammatory cell infiltration, ß-catenin, and cell proliferation marker (Ki67) in the colon were elevated > 60% in the HFD (45 % energy fat) group compared to the control (16 % energy fat) group. Furthermore, the content of Alistipes bacteria, the Firmicutes/Bacteroidetes ratio, microRNA-29a, and DCAs and LCAs (secondary BAs with oncogenic potential) were 50% greater in the feces of the HFD group compared to the control group. In summary, our multimodal profile data may represent a unique HFD-induced oncogenic signatures for colon health in a diet-induced mouse model. A greater understanding of these mechanistic action may open new avenues for seeking noninvasive colonic biomarkers.