<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wei L</submitter><funding>Flinders Foundation</funding><funding>NIDDK NIH HHS</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>NIAID NIH HHS</funding><funding>National Institutes of Health</funding><funding>European Commission</funding><funding>NIGMS NIH HHS</funding><funding>Australian Research Council</funding><pagination>2451-2466.e19</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8532026</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>160(7)</volume><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/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.&lt;h4>Methods&lt;/h4>We developed an inducible, EC cell-specific Tph1&lt;sup>CreERT2/+&lt;/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 </pubmed_abstract><journal>Gastroenterology</journal><pubmed_title>Serotonin Deficiency Is Associated With Delayed Gastric Emptying.</pubmed_title><pmcid>PMC8532026</pmcid><funding_grant_id>P01 DK041315</funding_grant_id><funding_grant_id>P30 GM110767</funding_grant_id><funding_grant_id>R01 DK103055</funding_grant_id><funding_grant_id>R01 DK094886</funding_grant_id><funding_grant_id>DP190103525</funding_grant_id><funding_grant_id>DK094886</funding_grant_id><funding_grant_id>P01 DK41315</funding_grant_id><funding_grant_id>R25 AI147369</funding_grant_id><funding_grant_id>DK103055</funding_grant_id><pubmed_authors>Keating DJ</pubmed_authors><pubmed_authors>Sanders KM</pubmed_authors><pubmed_authors>Spencer NJ</pubmed_authors><pubmed_authors>Habtezion A</pubmed_authors><pubmed_authors>Martin AM</pubmed_authors><pubmed_authors>Gottfried-Blackmore A</pubmed_authors><pubmed_authors>Jorgensen BG</pubmed_authors><pubmed_authors>Nguyen L</pubmed_authors><pubmed_authors>Chervo T</pubmed_authors><pubmed_authors>Jin B</pubmed_authors><pubmed_authors>Ro S</pubmed_authors><pubmed_authors>Ha SE</pubmed_authors><pubmed_authors>Singh R</pubmed_authors><pubmed_authors>Jones LA</pubmed_authors><pubmed_authors>Zogg H</pubmed_authors><pubmed_authors>Wei L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Serotonin Deficiency Is Associated With Delayed Gastric Emptying.</name><description>&lt;h4>Background &amp; aims&lt;/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.&lt;h4>Methods&lt;/h4>We developed an inducible, EC cell-specific Tph1&lt;sup>CreERT2/+&lt;/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 </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jun</publication><modification>2025-04-19T18:19:55.259Z</modification><creation>2025-04-19T18:19:55.259Z</creation></dates><accession>S-EPMC8532026</accession><cross_references><pubmed>33662386</pubmed><doi>10.1053/j.gastro.2021.02.060</doi></cross_references></HashMap>