{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T18:39:17Z","timestamp":1792003157296,"version":"4.4.0"},"reference-count":105,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,12,27]],"date-time":"2021-12-27T00:00:00Z","timestamp":1640563200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>A causal correlation between the metabolic disorders associated with sugar intake and disruption of the gastrointestinal (GI) homeostasis has been suggested, but the underlying mechanisms remain unclear. To unravel these mechanisms, we investigated the effect of physiological amounts of fructose and glucose on barrier functions and inflammatory status in various regions of the GI tract and on the cecal microbiota composition. C57BL\/6 mice were fed chow diet and given 15% glucose or 15% fructose in drinking water for 9 weeks. We monitored caloric intake, body weight, glucose intolerance, and adiposity. The intestinal paracellular permeability, cytokine, and tight junction protein expression were assessed in the jejunum, cecum, and colon. In the cecum, the microbiota composition was determined. Glucose-fed mice developed a marked increase in total adiposity, glucose intolerance, and paracellular permeability in the jejunum and cecum while fructose absorption did not affect any of these parameters. Fructose-fed mice displayed increased circulation levels of IL6. In the cecum, both glucose and fructose intake were associated with an increase in <jats:italic>Il13<\/jats:italic>, <jats:italic>Ifn\u03b3<\/jats:italic>, and <jats:italic>Tnf\u03b1<\/jats:italic> mRNA and MLCK protein levels. To clarify the relationships between monosaccharides and barrier function, we measured the permeability of Caco-2 cell monolayers in response to IFN\u03b3+TNF\u03b1 in the presence of glucose or fructose. <jats:italic>In vitro<\/jats:italic>, IFN\u03b3+TNF\u03b1-induced intestinal permeability increase was less pronounced in response to fructose than glucose. Mice treated with glucose showed an enrichment of <jats:italic>Lachnospiracae<\/jats:italic> and <jats:italic>Desulfovibrionaceae<\/jats:italic> while the fructose increased relative abundance of <jats:italic>Lactobacillaceae<\/jats:italic>. Correlations between pro-inflammatory cytokine gene expression and bacterial abundance highlighted the potential role of members of <jats:italic>Desulfovibrio<\/jats:italic> and <jats:italic>Lachnospiraceae NK4A136 group<\/jats:italic> genera in the inflammation observed in response to glucose intake. The increase in intestinal inflammation and circulating levels of IL6 in response to fructose was observed in the absence of intestinal permeability modification, suggesting that the intestinal permeability alteration does not precede the onset of metabolic outcome (low-grade inflammation, hyperglycemia) associated with chronic fructose consumption. The data also highlight the deleterious effects of glucose on gut barrier function along the GI tract and suggest that <jats:italic>Desulfovibrionaceae<\/jats:italic> and <jats:italic>Lachnospiraceae<\/jats:italic> play a key role in the onset of GI inflammation in response to glucose.<\/jats:p>","DOI":"10.3389\/fimmu.2021.742584","type":"journal-article","created":{"date-parts":[[2021,12,27]],"date-time":"2021-12-27T12:48:24Z","timestamp":1640609304000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":49,"title":["Glucose but Not Fructose Alters the Intestinal Paracellular Permeability in Association With Gut Inflammation and Dysbiosis in Mice"],"prefix":"10.3389","volume":"12","author":[{"given":"Xufei","family":"Zhang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magali","family":"Monnoye","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahendra","family":"Mariadassou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabienne","family":"Beguet-Crespel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Lapaque","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine","family":"Heberden","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Veronique","family":"Douard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,12,27]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1017\/S1368980013000141","article-title":"Sugar Consumption and Global Prevalence of Obesity and Hypertension: An Ecological Analysis","volume":"17","author":"Siervo","year":"2014","journal-title":"Public Health Nutr"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.3945\/ajcn.113.079533","article-title":"Glycemic Index, Glycemic Load, and Risk of Type 2 Diabetes: Results From 3 Large US Cohorts and an Updated Meta-Analysis","volume":"100","author":"Bhupathiraju","year":"2014","journal-title":"Am J Clin Nutr"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.2105\/AJPH.2012.300974","article-title":"Relationship of Soft Drink Consumption to Global Overweight, Obesity, and Diabetes: A Cross-National Analysis of 75 Countries","volume":"103","author":"Basu","year":"2013","journal-title":"Am J Public Health"},{"key":"B4","doi-asserted-by":"publisher","first-page":"e7492","DOI":"10.1136\/bmj.e7492","article-title":"Dietary Sugars and Body Weight: Systematic Review and Meta-Analyses of Randomised Controlled Trials and Cohort Studies","volume":"346","author":"Te Morenga","year":"2012","journal-title":"BMJ (Clinical Res)"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.2337\/dc13-2085","article-title":"Dietary Sugar and Body Weight: Have We Reached a Crisis in the Epidemic of Obesity and Diabetes? 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