{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wei L"],"funding":["Flinders Foundation","NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","NIAID NIH HHS","National Institutes of Health","European Commission","NIGMS NIH HHS","Australian Research Council"],"pagination":["2451-2466.e19"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8532026"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["160(7)"],"pubmed_abstract":["<h4>Background & aims</h4>Gastrointestinal (GI) motility is regulated by serotonin (5-hydroxytryptamine [5-HT]), which is primarily produced by enterochromaffin (EC) cells in the GI tract. However, the precise roles of EC cell-derived 5-HT in regulating gastric motility remain a major point of conjecture. Using a novel transgenic mouse line, we investigated the distribution of EC cells and the pathophysiologic roles of 5-HT deficiency in gastric motility in mice and humans.<h4>Methods</h4>We developed an inducible, EC cell-specific Tph1<sup>CreERT2/+</sup> mouse, which was used to generate a reporter mouse line, Tph1-tdTom, and an EC cell-depleted line, Tph1-DTA. We examined EC cell distribution, morphology, and subpopulations in reporter mice. GI motility was measured in vivo and ex vivo "],"journal":["Gastroenterology"],"pubmed_title":["Serotonin Deficiency Is Associated With Delayed Gastric Emptying."],"pmcid":["PMC8532026"],"funding_grant_id":["P01 DK041315","P30 GM110767","R01 DK103055","R01 DK094886","DP190103525","DK094886","P01 DK41315","R25 AI147369","DK103055"],"pubmed_authors":["Keating DJ","Sanders KM","Spencer NJ","Habtezion A","Martin AM","Gottfried-Blackmore A","Jorgensen BG","Nguyen L","Chervo T","Jin B","Ro S","Ha SE","Singh R","Jones LA","Zogg H","Wei L"],"additional_accession":[]},"is_claimable":false,"name":"Serotonin Deficiency Is Associated With Delayed Gastric Emptying.","description":"<h4>Background & aims</h4>Gastrointestinal (GI) motility is regulated by serotonin (5-hydroxytryptamine [5-HT]), which is primarily produced by enterochromaffin (EC) cells in the GI tract. However, the precise roles of EC cell-derived 5-HT in regulating gastric motility remain a major point of conjecture. Using a novel transgenic mouse line, we investigated the distribution of EC cells and the pathophysiologic roles of 5-HT deficiency in gastric motility in mice and humans.<h4>Methods</h4>We developed an inducible, EC cell-specific Tph1<sup>CreERT2/+</sup> mouse, which was used to generate a reporter mouse line, Tph1-tdTom, and an EC cell-depleted line, Tph1-DTA. We examined EC cell distribution, morphology, and subpopulations in reporter mice. GI motility was measured in vivo and ex vivo ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2025-04-19T18:19:55.259Z","creation":"2025-04-19T18:19:55.259Z"},"accession":"S-EPMC8532026","cross_references":{"pubmed":["33662386"],"doi":["10.1053/j.gastro.2021.02.060"]}}