ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2017
FFA2 activation combined with ulcerogenic COX inhibition induces duodenal mucosal injury via the 5-HT pathway in rats.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Enterochromaffin Cells: Sentinels to Gut Microbiota in Hyperalgesia?Frontiers in cellular and infection microbiology · 2021Pooled it
- The IL-18 receptor is expressed on murine small-intestinal enterochromaffin cells and executes a recovery program upon injury.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Shaoyao Decoction reduced T lymphocyte activation by regulating of intestinal flora and 5-hydroxytryptamine metabolism in ulcerative colitis.Chinese medicine · 2024Article
- Intestinal FFA2 promotes obesity by altering food intake in Western diet-fed mice.The Journal of endocrinology · 2024Article
- Gastroparesis Worsens Indomethacin-Induced Gastric Antral Ulcers by Bile Reflux via Activation of 5-HTDigestive diseases and sciences · 2023Article
- Effect of the gut microbiota and their metabolites on postoperative intestinal motility and its underlying mechanisms.Journal of translational medicine · 2023Review
- The possible role of gut microbiota dysbiosis in the pathophysiology of delirium in older persons.Microbiome research reports · 2023Review
- The Role of Short Chain Fatty Acids in Irritable Bowel Syndrome.Journal of neurogastroenterology and motility · 2022Review
- A Focus on Enterochromaffin Cells among the Enteroendocrine Cells: Localization, Morphology, and Role.International journal of molecular sciences · 2022Review
- Potential Roles of Enterochromaffin Cells in Early Life Stress-Induced Irritable Bowel Syndrome.Frontiers in cellular neuroscience · 2022Review
- Gut Microbiota in NSAID Enteropathy: New Insights From Inside.Frontiers in cellular and infection microbiology · 2021Review
- Mouse Abdominal Fat Depots Reduced by Butyric Acid-ProducingMicroorganisms · 2020Article
- Leuconostoc mesenteroides fermentation produces butyric acid and mediates Ffar2 to regulate blood glucose and insulin in type 1 diabetic mice.Scientific reports · 2020Article
- Duodenal Chemosensing of Short-Chain Fatty Acids: Implications for GI Diseases.Current gastroenterology reports · 2019Review
- Duodenal chemosensing.Current opinion in gastroenterology · 2018Review
- Enterochromaffin 5-HT cells - A major target for GLP-1 and gut microbial metabolites.Molecular metabolism · 2018Article
- Luminal chemosensing in the gastroduodenal mucosa.Current opinion in gastroenterology · 2017Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Serotonin (5-HT), predominantly synthesized and released by enterochromaffin cells, is implicated in gastrointestinal symptoms such as emesis, abdominal pain, and diarrhea. Because luminal short-chain fatty acids (SCFAs) release 5-HT from enterochromaffin cells, which express the SCFA receptor free fatty acid receptor 2 (FFA2) in rat duodenum, we examined the effects of the selective FFA2 agonist phenylacetamide-1 (PA1) on duodenal 5-HT release with consequent bicarbonate secretion [duodenal bicarbonate secretion (DBS)] and on indomethacin (IND)-induced enteropathy. Intestinal injury was induced by IND (10 mg/kg sc) with or without PA1. We measured DBS in vivo in a duodenal loop perfused with PA1 while measuring 5-HT released in the portal vein. Duodenal blood flow was measured by laser-Doppler flowmetry. IND induced small intestinal ulcers with duodenal sparing. PA1 given with IND (IND + PA1) dose dependently induced duodenal erosions. IND + PA1-induced duodenal lesions were inhibited by the FFA2 antagonist GLPG-0974, ondansetron, or omeprazole but not by RS-23597 or atropine. Luminal perfusion of PA1 augmented DBS accompanied by increased portal blood 5-HT concentrations with approximately eight times more release at 0.1 mM than at 1 µM, with the effects inhibited by coperfusion of GLPG-0974. Luminal PA1 at 1 µM increased, but at 0.1 mM diminished, duodenal blood flow. Cosuperfusion of PA1 (0.1 mM) decreased acid-induced hyperemia, further reduced by IND pretreatment but restored by ondansetron. These results suggest that, although FFA2 activation enhances duodenal mucosal defenses, FFA2 overactivation during ulcerogenic cyclooxygenase inhibition may increase the vulnerability of the duodenal mucosa to gastric acid via excessive 5-HT release and 5-HT
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