Cross Talk between Apical Periodontitis and Metabolic Disorders: Experimental Evidence on the Role of Intestinal Adipokines and Akkermansia muciniphila
| Autor: | Helena Schirmer, Bruno Silveira Adami, Maria M. Campos, André Arigony Souto, José Antônio Poli de Figueiredo, Fernanda Letícia Rost, Rodrigo B. M. Silva, Ana Paula Aquistapase Dagnino, Fábio Luiz Dal Moro Maito, Cauana Oliva Tavares |
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| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Adipokine Inflammation 03 medical and health sciences 0302 clinical medicine Adipokines Metabolic Diseases Verrucomicrobia Internal medicine medicine Animals Intestinal Mucosa Rats Wistar Interleukin 6 General Dentistry biology Adiponectin business.industry Leptin 030206 dentistry biology.organism_classification medicine.disease Gastrointestinal Microbiome Disease Models Animal 030104 developmental biology Endocrinology biology.protein medicine.symptom Metabolic syndrome business Dysbiosis Periapical Periodontitis Akkermansia muciniphila |
| Zdroj: | Journal of Endodontics. 45:174-180 |
| ISSN: | 0099-2399 |
| Popis: | Introduction Infection and dysbiosis present a close relationship with metabolic diseases although the influence of apical periodontitis (AP) in this context needs further investigation. This study evaluated the influence of AP in a rat model of metabolic syndrome induced by 10% fructose supplementation. Methods Male Wistar rats were used. Animals that received a high-fructose diet (HFD, n = 30) or filtered water (control, n = 30) were subdivided into the following groups: (1) without induction of AP (no AP, n = 10 each), (2) with AP induction 2 weeks before euthanasia (AP 14 days, n = 10 each), and (3) with AP induction 4 weeks before euthanasia (AP 28 days, n = 10 each). Results HFD triggered metabolic syndrome, as indicated by the induction of overweight and hyperglycemia, besides polydipsia, regardless of the AP induction. Serum or intestinal tumor necrosis factor, interleukin 1 beta, and interleukin 6 levels were undetectable, regardless of the experimental group. Serum leptin and adiponectin levels were significantly elevated in the HFD group without AP induction. The intestinal levels of leptin were significantly increased in the groups with 28 days of AP induction despite HFD. A significant elevation of liver glutathione levels was observed in animals submitted to HFD and AP for 14 days. AP induction (14 or 28 days) led to pulp and periapical tissue inflammation without any influence of HFD. Either HFD or AP induction led to dysbiosis, as indicated by a significant reduction of fecal A. muciniphila expression. Conclusions We provide novel evidence that AP can have systemic impacts on metabolic disorders, likely by modulating intestinal metabolism and microbiota. |
| Databáze: | OpenAIRE |
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