{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:16:37Z","timestamp":1787015797915,"version":"build-2736575974"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2020,8,9]],"date-time":"2020-08-09T00:00:00Z","timestamp":1596931200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>There is increased recognition of duodenal disturbances (inflammation, altered mucosal protein expression, and chemosensitivity) in functional dyspepsia (FD). Besides sensorimotor functions, enteric submucosal neurons also regulate epithelial ion transport. We hypothesized that duodenal mucosal ion transport and expression of associated genes are altered in FD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Duodenal mucosal ion transport (basal and acetylcholine\u2010 and glucose\u2010evoked changes in short\u2010circuit current [Isc]) and expression of associated genes and regulatory miRNAs were evaluated in 40 FD patients and 24 healthy controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Basal Isc (FD: 88.2 [52.6]\u00a0\u03bcA\/cm\n                      <jats:sup>2<\/jats:sup>\n                      vs healthy: 20.3 [50.2]\u00a0\u03bcA\/cm\n                      <jats:sup>2<\/jats:sup>\n                      ;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0\u2264\u00a0.0001), acetylcholine\u2010evoked Isc (FD: Emax 50.4 [35.8]\u00a0\u03bcA\/cm\n                      <jats:sup>2<\/jats:sup>\n                      vs healthy: 16.6 [15]\u00a0\u03bcA\/cm\n                      <jats:sup>2<\/jats:sup>\n                      ;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0\u2264\u00a0.001), and glucose\u2010evoked Isc responses (FD: E\n                      <jats:sub>max<\/jats:sub>\n                      69.8 [42.1]\u00a0\u03bcA\/cm\n                      <jats:sup>2<\/jats:sup>\n                      vs healthy: 40.3 [24.6]\u00a0\u03bcA\/cm\n                      <jats:sup>2<\/jats:sup>\n                      ;\n                      <jats:italic>P<\/jats:italic>\n                      \u00a0=\u00a0.02) were greater in FD than in controls. The Emax for glucose was greater in FD patients on selective serotonin reuptake inhibitors. In FD, the mRNA expression of\n                      <jats:italic>SLC4A7<\/jats:italic>\n                      and\n                      <jats:italic>SLC4A4<\/jats:italic>\n                      , which transport bicarbonate into cells at the basolateral surface, and the apical anion exchanger\n                      <jats:italic>SLC26A3<\/jats:italic>\n                      were reduced (false discovery rate &lt;0.05), the serotonin receptor\n                      <jats:italic>HTR4<\/jats:italic>\n                      was increased, and the serotonin transporter\n                      <jats:italic>SLC6A4<\/jats:italic>\n                      was decreased. Selected miRNAs (hsa\u2010miR\u2010590\u20103p, hsa\u2010miR\u201032\u20105p) that target genes associated with ionic transport were upregulated in FD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Compared to controls, FD patients had greater baseline and agonist\u2010evoked duodenal mucosal secretory responses. These findings may be explained by reduced gene expression, which would be anticipated to reduce luminal bicarbonate secretion. The upregulated miRNAs may partly explain the downregulation of these genes in FD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nmo.13955","type":"journal-article","created":{"date-parts":[[2020,8,10]],"date-time":"2020-08-10T01:53:34Z","timestamp":1597024414000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Duodenal mucosal secretory disturbances in functional dyspepsia"],"prefix":"10.1111","volume":"33","author":[{"given":"Susrutha","family":"Puthanmadhom Narayanan","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology Mayo Clinic Rochester MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1727-0387","authenticated-orcid":false,"given":"David R.","family":"Linden","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biomedical Engineering Mayo Clinic Rochester MN 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