{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T20:10:22Z","timestamp":1792008622088,"version":"4.4.0"},"reference-count":40,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2021,8,21]],"date-time":"2021-08-21T00:00:00Z","timestamp":1629504000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and Aim<\/jats:title><jats:p>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\u2010like ileitis. We aimed to investigate the effect of ACK on the intestinal mucosa and gut microbiota of normal mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Acesulfame potassium was administered to C57BL\/6J mice (8\u00a0weeks old) via free drinking. Intestinal damage was evaluated histologically, and messenger RNA (mRNA) levels of TNF\u2010\u03b1, IFN\u2010\u03b3, IL1\u2010\u03b2, MAdCAM\u20101, GLP1R, and GLP2R were determined with quantitative reverse transcription polymerase chain reaction (qRT\u2010PCR). Immunohistochemistry was performed to examine the expression of MAdCAM\u20101 in the small intestine. The composition of gut microbiota was assessed using high\u2010throughput sequencing. We performed intravital microscopic observation to examine if ACK altered lymphocyte migration to the intestinal microvessels.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Acesulfame potassium increased the expression of proinflammatory cytokines, decreased the expression of GLP\u20101R and GLP\u20102R, 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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa. Massive use of non\u2010caloric artificial sweeteners may not be as safe as we think.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.15654","type":"journal-article","created":{"date-parts":[[2021,8,9]],"date-time":"2021-08-09T05:25:35Z","timestamp":1628486735000},"page":"3140-3148","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa"],"prefix":"10.1111","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7576-7538","authenticated-orcid":false,"given":"Yoshinori","family":"Hanawa","sequence":"first","affiliation":[{"name":"Department of Internal Medicine National Defense Medical College  Saitama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaaki","family":"Higashiyama","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine National Defense 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