Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa
| Autor: | Masaaki Higashiyama, Akinori Mizoguchi, Chie Kurihara, Rina Tanemoto, Yoshikiyo Okada, Nao Sugihara, Yoshinori Hanawa, Kenichi Inaba, Kazuyuki Narimatsu, Shunsuke Komoto, Ryota Hokari, Akinori Wada, Kazuki Horiuchi, Shin Nishii, Kengo Tomita, Suguru Ito |
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| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
Thiazines Acesulfame potassium Gut flora Proinflammatory cytokine Mice chemistry.chemical_compound Intestinal mucosa Cell Movement Internal medicine medicine Animals Ileitis Lymphocytes Intestinal Mucosa Intestinal permeability Hepatology biology business.industry Gastroenterology medicine.disease biology.organism_classification Small intestine Intestines Mice Inbred C57BL medicine.anatomical_structure Endocrinology chemistry Sweetening Agents Dysbiosis business |
| Zdroj: | Journal of Gastroenterology and Hepatology. 36:3140-3148 |
| ISSN: | 1440-1746 0815-9319 |
| Popis: | BACKGROUND AND AIM The artificial sweetener acesulfame potassium (ACK) is officially approved as safe for intake and has been used in processed foods. However, ACKs have been reported to induce metabolic syndrome, along with alteration of the gut microbiota in mice. In recent years, studies have suggested that this artificial sweetener promotes myeloperoxidase reactivity in Crohn's disease-like ileitis. We aimed to investigate the effect of ACK on the intestinal mucosa and gut microbiota of normal mice. METHODS Acesulfame potassium was administered to C57BL/6J mice (8 weeks old) via free drinking. Intestinal damage was evaluated histologically, and messenger RNA (mRNA) levels of TNF-α, IFN-γ, IL1-β, MAdCAM-1, GLP1R, and GLP2R were determined with quantitative reverse transcription polymerase chain reaction (qRT-PCR). Immunohistochemistry was performed to examine the expression of MAdCAM-1 in the small intestine. The composition of gut microbiota was assessed using high-throughput sequencing. We performed intravital microscopic observation to examine if ACK altered lymphocyte migration to the intestinal microvessels. RESULTS Acesulfame potassium increased the expression of proinflammatory cytokines, decreased the expression of GLP-1R and GLP-2R, and induced small intestinal injury with an increase in intestinal permeability, and ACK treatment induced microbial changes, but the transfer of feces alone from ACK mice did not reproduce intestinal damage in recipient mice. ACK treatment significantly increased the migration of lymphocytes to intestinal microvessels. CONCLUSION Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa. Massive use of non-caloric artificial sweeteners may not be as safe as we think. |
| Databáze: | OpenAIRE |
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