High-Fructose Diet Alters Intestinal Microbial Profile and Correlates with Early Tumorigenesis in a Mouse Model of Barrett's Esophagus

التفاصيل البيبلوغرافية
العنوان: High-Fructose Diet Alters Intestinal Microbial Profile and Correlates with Early Tumorigenesis in a Mouse Model of Barrett's Esophagus
المؤلفون: Amira Metwaly, Katja Steiger, Julia Strangmann, Michael Quante, Andrea Proaño-Vasco, Theresa Baumeister, Sandra Reitmeier, Timothy C. Wang, Roland Rad, Thomas Engleitner, Rupert Öllinger, Michael Gigl, Robert Thimme, Roland M. Schmid, Chen Meng, Akanksha Anand, Karin Kleigrewe
المصدر: Microorganisms
Microorganisms, Vol 9, Iss 2432, p 2432 (2021)
Microorganisms; Volume 9; Issue 12; Pages: 2432
سنة النشر: 2021
مصطلحات موضوعية: Microbiology (medical), medicine.medical_specialty, esophageal adenocarcinoma, QH301-705.5, Gut flora, medicine.disease_cause, Microbiology, digestive system, Article, fructose, chemistry.chemical_compound, Virology, Internal medicine, medicine, microbiota, Barrett’s esophagus, Biology (General), Western diet, biology, Cell growth, Fructose, Metabolism, biology.organism_classification, medicine.disease, Phenotype, IL-1B-mouse model, medicine.anatomical_structure, Endocrinology, chemistry, Barrett's esophagus, Carcinogenesis, Pancreas, metabolism
الوصف: Esophageal adenocarcinoma (EAC) is mostly prevalent in industrialized countries and has been associated with obesity, commonly linked with a diet rich in fat and refined sugars containing high fructose concentrations. In meta-organisms, dietary components are digested and metabolized by the host and its gut microbiota. Fructose has been shown to induce proliferation and cell growth in pancreas and colon cancer cell lines and also alter the gut microbiota. In a previous study with the L2-IL-1B mouse model, we showed that a high-fat diet (HFD) accelerated EAC progression from its precursor lesion Barrett’s esophagus (BE) through changes in the gut microbiota. Aiming to investigate whether a high-fructose diet (HFrD) also alters the gut microbiota and favors EAC carcinogenesis, we assessed the effects of HFrD on the phenotype and intestinal microbial communities of L2-IL1B mice. Results showed a moderate acceleration in histologic disease progression, a mild effect on the systemic inflammatory response, metabolic changes in the host, and a shift in the composition, metabolism, and functionality of intestinal microbial communities. We conclude that HFrD alters the overall balance of the gut microbiota and induces an acceleration in EAC progression in a less pronounced manner than HFD.
وصف الملف: application/pdf
تدمد: 2076-2607
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9bbe0a2f85cb50f3b728f4cab8665730
https://pubmed.ncbi.nlm.nih.gov/34946037
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....9bbe0a2f85cb50f3b728f4cab8665730
قاعدة البيانات: OpenAIRE