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Diet-Induced Non-alcoholic Fatty Liver Disease and Associated Gut Dysbiosis Are Exacerbated by Oral Infection.
Simas, Alexandra M; Kramer, Carolyn D; Genco, Caroline A.
Afiliação
  • Simas AM; Gerald J. and Dorothy R. Friedman School of Nutrition and Science Policy, Graduate Program in Biochemical and Molecular Nutrition, Tufts University, Boston, MA, United States.
  • Kramer CD; Department of Immunology, Tufts University School of Medicine, Boston, MA, United States.
  • Genco CA; Department of Immunology, Tufts University School of Medicine, Boston, MA, United States.
Front Oral Health ; 2: 784448, 2021.
Article em En | MEDLINE | ID: mdl-35141703
ABSTRACT
Increasing evidence indicates that chronic inflammation due to periodontal disease is associated with progression of non-alcoholic fatty liver disease (NAFLD) caused by a Western diet. NAFLD has also been associated with oral infection with the etiological agent of periodontal disease, Porphyromonas gingivalis. P. gingivalis oral infection has been shown to induce cardiometabolic disease features including hepatic lipid accumulation while also leading to dysbiosis of the gut microbiome. However, the impact of P. gingivalis infection on the gut microbiota of mice with diet-induced NAFLD and the potential for those changes to mediate NAFLD progression has yet to be determined. In the current study, we have demonstrated that P. gingivalis infection induced sustained alterations of the gut microbiota composition and predicted functions, which was associated with the promotion of NAFLD in steatotic mice. Reduced abundance of short-chain fatty acid-producing microbiota was observed after both acute and chronic P. gingivalis infection. Collectively, our findings demonstrate that P. gingivalis infection produces a persistent change in the gut microbiota composition and predicted functions that promotes steatosis and metabolic disease.
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Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2021 Tipo de documento: Article