ArticleNutrients2020
Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3.
Article in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- The Impact of Non-caloric Sweeteners on Male Fertility: A Systematic Review and Narrative Synthesis in Rodent Models.Frontiers in nutrition · 2022Pooled it
- Mechanism-First Psychobiotics: Fermented Vegetables, Dairy, and Soy for Depression and Anxiety.International journal of molecular sciences · 2026Review
- Targeting sweet taste receptor T1R2/T1R3: a new strategy for metabolic disease regulation and intervention of multiple organ diseases.Food chemistry. Molecular sciences · 2026Review
- Artificial Sweeteners and Autoimmune Diseases: Insights From Integrative Bioinformatics and Mendelian Randomization.Food science & nutrition · 2026Article
- Phenolic Compounds of Grape Pomace Skin Released During SHIME Colonic Fermentation Shape the Transcriptomic Profile of Tight Junctions, Improving the Barrier Properties in Caco-2 Cells.International journal of molecular sciences · 2026Article
- Sucralose and the Gut-Immune Axis: Emerging Evidence Linking Dysbiosis, Barrier Alterations, and Implications for Colitis and Colorectal Cancer Immunotherapy.Biomedicines · 2026Review
- In Vitro Testing of Artificial Sweeteners with Apple and Chokeberry Fruit Juice Extracts for Intestinal Permeability and Glucose Uptake.ACS omega · 2026Article
- Processed Diets and Food Additives Shape the Gut Microbiota and Chronic Disease Risk Across the Life Course-A Three-Layer Ecosystem Disruption Model (TLED) Model.Life (Basel, Switzerland) · 2026Review
- Attention-deficit/hyperactivity disorder is associated with increased consumption of ultra-processed foods among children.Pediatric research · 2026Article
- Cellular Stress, Inflammation and Barrier Damage in Gut Epithelial Cells Caused by Aspartame.Allergy · 2026Article
- Pneumococcal Endopeptidase O Attenuates Colitis by Inhibiting the Macrophage-CCL2 Axis and Reshaping Gut Microbiota.Journal of inflammation research · 2026Article
- Non-nutritive sweeteners, the gut microbiome, and tumor immunity: evidence hierarchy and a sucralose-centered translational model.Frontiers in nutrition · 2026Review
- The non-synthetic sweeteners, miraculin and mogroside V, but not stevia, disrupt the intestinal epithelial barrier function through a sweet taste receptor-dependent mechanism.Scientific reports · 2025Article
- Disrupting the Gut-Brain Axis: How Artificial Sweeteners Rewire Microbiota and Reward Pathways.International journal of molecular sciences · 2025Review
- Ultra-processed foods: Implications for gastrointestinal health.World journal of gastroenterology · 2025Review
- Biological and Behavioral Responses ofInternational journal of molecular sciences · 2025Article
- Investigating the Impact of Aspartame on Ulcerative Colitis Through Network Toxicology and Molecular Docking.Food science & nutrition · 2025Article
- Long-Term Exposure to Sucrose during the Differentiation Process Increases Permeability Independently of TAS1R3 in In Vitro Models of the Intestinal Barrier Function.Journal of agricultural and food chemistry · 2025Article
- Glycemic response to SSBs and ASBs: the role of mixed meals and individual variability.Nutrition journal · 2025Article
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The breakdown of the intestinal epithelial barrier and subsequent increase in intestinal permeability can lead to systemic inflammatory diseases and multiple-organ failure. Nutrition impacts the intestinal barrier, with dietary components such as gluten increasing permeability. Artificial sweeteners are increasingly consumed by the general public in a range of foods and drinks. The sweet taste receptor (T1R3) is activated by artificial sweeteners and has been identified in the intestine to play a role in incretin release and glucose transport; however, T1R3 has not been previously linked to intestinal permeability. Here, the intestinal epithelial cell line, Caco-2, was used to study the effect of commonly-consumed artificial sweeteners, sucralose, aspartame and saccharin, on permeability. At high concentrations, aspartame and saccharin were found to induce apoptosis and cell death in intestinal epithelial cells, while at low concentrations, sucralose and aspartame increased epithelial barrier permeability and down-regulated claudin 3 at the cell surface. T1R3 knockdown was found to attenuate these effects of artificial sweeteners. Aspartame induced reactive oxygen species (ROS) production to cause permeability and claudin 3 internalization, while sweetener-induced permeability and oxidative stress was rescued by the overexpression of claudin 3. Taken together, our findings demonstrate that the artificial sweeteners sucralose, aspartame, and saccharin exert a range of negative effects on the intestinal epithelium through the sweet taste receptor T1R3.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.