Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa
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 sug...
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| Veröffentlicht in: | Journal of gastroenterology and hepatology 2021-11, Vol.36 (11), p.3140-3148 |
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| creator | Hanawa, Yoshinori Higashiyama, Masaaki Kurihara, Chie Tanemoto, Rina Ito, Suguru Mizoguchi, Akinori Nishii, Shin Wada, Akinori Inaba, Kenichi Sugihara, Nao Horiuchi, Kazuki Okada, Yoshikiyo Narimatsu, Kazuyuki Komoto, Shunsuke Tomita, Kengo Hokari, Ryota |
| description | 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. |
| doi_str_mv | 10.1111/jgh.15654 |
| format | Article |
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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.</description><identifier>ISSN: 0815-9319</identifier><identifier>EISSN: 1440-1746</identifier><identifier>DOI: 10.1111/jgh.15654</identifier><identifier>PMID: 34368996</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>acesulfame potassium ; Animals ; artificial sweetener ; Artificial sweeteners ; Cell Movement ; Crohn's disease ; Digestive system ; Dysbacteriosis ; dysbiosis ; Dysbiosis - chemically induced ; Food processing ; Gastrointestinal tract ; Ileitis ; Immunohistochemistry ; Inflammation ; Interferon ; Interleukin 1 ; intestinal inflammation ; Intestinal microflora ; Intestinal Mucosa ; Intestines - injuries ; Leukocyte migration ; Lymphocytes ; Metabolic syndrome ; Mice ; Mice, Inbred C57BL ; Microbiota ; migration ; Mucosa ; Permeability ; Peroxidase ; Polymerase chain reaction ; Potassium ; Reverse transcription ; Small intestine ; Sweeteners ; Sweetening Agents - toxicity ; Thiazines - toxicity ; Tumor necrosis factor</subject><ispartof>Journal of gastroenterology and hepatology, 2021-11, Vol.36 (11), p.3140-3148</ispartof><rights>2021 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd</rights><rights>2021 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3534-d41addde9df25d4c471e9acfccf5945703c7143bae6cf6dd7da09dc73ce736863</citedby><cites>FETCH-LOGICAL-c3534-d41addde9df25d4c471e9acfccf5945703c7143bae6cf6dd7da09dc73ce736863</cites><orcidid>0000-0002-8511-2540 ; 0000-0001-7576-7538</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjgh.15654$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjgh.15654$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34368996$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hanawa, Yoshinori</creatorcontrib><creatorcontrib>Higashiyama, Masaaki</creatorcontrib><creatorcontrib>Kurihara, Chie</creatorcontrib><creatorcontrib>Tanemoto, Rina</creatorcontrib><creatorcontrib>Ito, Suguru</creatorcontrib><creatorcontrib>Mizoguchi, Akinori</creatorcontrib><creatorcontrib>Nishii, Shin</creatorcontrib><creatorcontrib>Wada, Akinori</creatorcontrib><creatorcontrib>Inaba, Kenichi</creatorcontrib><creatorcontrib>Sugihara, Nao</creatorcontrib><creatorcontrib>Horiuchi, Kazuki</creatorcontrib><creatorcontrib>Okada, Yoshikiyo</creatorcontrib><creatorcontrib>Narimatsu, Kazuyuki</creatorcontrib><creatorcontrib>Komoto, Shunsuke</creatorcontrib><creatorcontrib>Tomita, Kengo</creatorcontrib><creatorcontrib>Hokari, Ryota</creatorcontrib><title>Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa</title><title>Journal of gastroenterology and hepatology</title><addtitle>J Gastroenterol Hepatol</addtitle><description>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.</description><subject>acesulfame potassium</subject><subject>Animals</subject><subject>artificial sweetener</subject><subject>Artificial sweeteners</subject><subject>Cell Movement</subject><subject>Crohn's disease</subject><subject>Digestive system</subject><subject>Dysbacteriosis</subject><subject>dysbiosis</subject><subject>Dysbiosis - chemically induced</subject><subject>Food processing</subject><subject>Gastrointestinal tract</subject><subject>Ileitis</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interleukin 1</subject><subject>intestinal inflammation</subject><subject>Intestinal microflora</subject><subject>Intestinal Mucosa</subject><subject>Intestines - injuries</subject><subject>Leukocyte migration</subject><subject>Lymphocytes</subject><subject>Metabolic syndrome</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microbiota</subject><subject>migration</subject><subject>Mucosa</subject><subject>Permeability</subject><subject>Peroxidase</subject><subject>Polymerase chain reaction</subject><subject>Potassium</subject><subject>Reverse transcription</subject><subject>Small intestine</subject><subject>Sweeteners</subject><subject>Sweetening Agents - toxicity</subject><subject>Thiazines - toxicity</subject><subject>Tumor necrosis factor</subject><issn>0815-9319</issn><issn>1440-1746</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1LAzEQhoMoWqsH_4AEvOhhbbL5ao5StFUKXvS8pEm2Tdnd1M2Gsv_e1FYRwbnMMDzzMjMvAFcY3eMUo_VydY8ZZ_QIDDClKMOC8mMwQGPMMkmwPAPnIawRQhQJdgrOCCV8LCUfgO5B2xCrUtUWbnynQnCxhq4xMfWh6cPC-eACVI1J3c6GzjWqSuU6tj3cum4FbbNSjbYGVn29WXnddxbWbtmqzvkGdv73XB21D-oCnJSqCvbykIfg_enxbTLL5q_T58nDPNOEEZoZipUxxkpT5sxQTQW2UulS65JJygQiWmBKFspyXXJjhFFIGi2ItiLdx8kQ3O51N63_iGmHonZB26pSjfUxFDljknOKZZ7Qmz_o2sc2rbyjJJUyF_k4UXd7Src-hNaWxaZ1tWr7AqNiZ0WRrCi-rEjs9UExLmprfsjv3ydgtAe2rrL9_0rFy3S2l_wEwqOWNA</recordid><startdate>202111</startdate><enddate>202111</enddate><creator>Hanawa, Yoshinori</creator><creator>Higashiyama, Masaaki</creator><creator>Kurihara, Chie</creator><creator>Tanemoto, Rina</creator><creator>Ito, Suguru</creator><creator>Mizoguchi, Akinori</creator><creator>Nishii, Shin</creator><creator>Wada, Akinori</creator><creator>Inaba, Kenichi</creator><creator>Sugihara, Nao</creator><creator>Horiuchi, Kazuki</creator><creator>Okada, Yoshikiyo</creator><creator>Narimatsu, Kazuyuki</creator><creator>Komoto, Shunsuke</creator><creator>Tomita, Kengo</creator><creator>Hokari, Ryota</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8511-2540</orcidid><orcidid>https://orcid.org/0000-0001-7576-7538</orcidid></search><sort><creationdate>202111</creationdate><title>Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa</title><author>Hanawa, Yoshinori ; Higashiyama, Masaaki ; Kurihara, Chie ; Tanemoto, Rina ; Ito, Suguru ; Mizoguchi, Akinori ; Nishii, Shin ; Wada, Akinori ; Inaba, Kenichi ; Sugihara, Nao ; Horiuchi, Kazuki ; Okada, Yoshikiyo ; Narimatsu, Kazuyuki ; Komoto, Shunsuke ; Tomita, Kengo ; Hokari, Ryota</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3534-d41addde9df25d4c471e9acfccf5945703c7143bae6cf6dd7da09dc73ce736863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>acesulfame potassium</topic><topic>Animals</topic><topic>artificial sweetener</topic><topic>Artificial sweeteners</topic><topic>Cell Movement</topic><topic>Crohn's disease</topic><topic>Digestive system</topic><topic>Dysbacteriosis</topic><topic>dysbiosis</topic><topic>Dysbiosis - chemically induced</topic><topic>Food processing</topic><topic>Gastrointestinal tract</topic><topic>Ileitis</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Interferon</topic><topic>Interleukin 1</topic><topic>intestinal inflammation</topic><topic>Intestinal microflora</topic><topic>Intestinal Mucosa</topic><topic>Intestines - injuries</topic><topic>Leukocyte migration</topic><topic>Lymphocytes</topic><topic>Metabolic syndrome</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microbiota</topic><topic>migration</topic><topic>Mucosa</topic><topic>Permeability</topic><topic>Peroxidase</topic><topic>Polymerase chain reaction</topic><topic>Potassium</topic><topic>Reverse transcription</topic><topic>Small intestine</topic><topic>Sweeteners</topic><topic>Sweetening Agents - toxicity</topic><topic>Thiazines - toxicity</topic><topic>Tumor necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hanawa, Yoshinori</creatorcontrib><creatorcontrib>Higashiyama, Masaaki</creatorcontrib><creatorcontrib>Kurihara, Chie</creatorcontrib><creatorcontrib>Tanemoto, Rina</creatorcontrib><creatorcontrib>Ito, Suguru</creatorcontrib><creatorcontrib>Mizoguchi, Akinori</creatorcontrib><creatorcontrib>Nishii, Shin</creatorcontrib><creatorcontrib>Wada, Akinori</creatorcontrib><creatorcontrib>Inaba, Kenichi</creatorcontrib><creatorcontrib>Sugihara, Nao</creatorcontrib><creatorcontrib>Horiuchi, Kazuki</creatorcontrib><creatorcontrib>Okada, Yoshikiyo</creatorcontrib><creatorcontrib>Narimatsu, Kazuyuki</creatorcontrib><creatorcontrib>Komoto, Shunsuke</creatorcontrib><creatorcontrib>Tomita, Kengo</creatorcontrib><creatorcontrib>Hokari, Ryota</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of gastroenterology and hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hanawa, Yoshinori</au><au>Higashiyama, Masaaki</au><au>Kurihara, Chie</au><au>Tanemoto, Rina</au><au>Ito, Suguru</au><au>Mizoguchi, Akinori</au><au>Nishii, Shin</au><au>Wada, Akinori</au><au>Inaba, Kenichi</au><au>Sugihara, Nao</au><au>Horiuchi, Kazuki</au><au>Okada, Yoshikiyo</au><au>Narimatsu, Kazuyuki</au><au>Komoto, Shunsuke</au><au>Tomita, Kengo</au><au>Hokari, Ryota</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa</atitle><jtitle>Journal of gastroenterology and hepatology</jtitle><addtitle>J Gastroenterol Hepatol</addtitle><date>2021-11</date><risdate>2021</risdate><volume>36</volume><issue>11</issue><spage>3140</spage><epage>3148</epage><pages>3140-3148</pages><issn>0815-9319</issn><eissn>1440-1746</eissn><abstract>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.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>34368996</pmid><doi>10.1111/jgh.15654</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8511-2540</orcidid><orcidid>https://orcid.org/0000-0001-7576-7538</orcidid></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | acesulfame potassium Animals artificial sweetener Artificial sweeteners Cell Movement Crohn's disease Digestive system Dysbacteriosis dysbiosis Dysbiosis - chemically induced Food processing Gastrointestinal tract Ileitis Immunohistochemistry Inflammation Interferon Interleukin 1 intestinal inflammation Intestinal microflora Intestinal Mucosa Intestines - injuries Leukocyte migration Lymphocytes Metabolic syndrome Mice Mice, Inbred C57BL Microbiota migration Mucosa Permeability Peroxidase Polymerase chain reaction Potassium Reverse transcription Small intestine Sweeteners Sweetening Agents - toxicity Thiazines - toxicity Tumor necrosis factor |
| title | Acesulfame potassium induces dysbiosis and intestinal injury with enhanced lymphocyte migration to intestinal mucosa |
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