{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:19:30Z","timestamp":1784557170771,"version":"3.55.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,2]]},"abstract":"<jats:p>\n                    Gastrin, secreted by stomach G cells in response to ingested sodium, stimulates the renal cholecystokinin B receptor (CCKBR) to increase renal sodium excretion. It is not known how dietary sodium, independent of food, can increase gastrin secretion in human G cells. However, fenofibrate (FFB), a peroxisome proliferator-activated receptor-\u03b1 (PPAR-\u03b1) agonist, increases gastrin secretion in rodents and several human gastrin-secreting cells, via a gastrin transcriptional promoter. We tested the following hypotheses: (1.) the sodium sensor in G cells plays a critical role in the sodium-mediated increase in gastrin expression\/secretion, and (2.) dopamine, via the D\n                    <jats:sub>1<\/jats:sub>\n                    R and PPAR-\u03b1, is involved. Intact human stomach antrum and G cells were compared with human gastrin-secreting gastric and ovarian adenocarcinoma cells. When extra- or intracellular sodium was increased in human antrum, human G cells, and adenocarcinoma cells, gastrin mRNA and protein expression\/secretion were increased. In human G cells, the PPAR-\u03b1 agonist FFB increased gastrin protein expression that was blocked by GW6471, a PPAR-\u03b1 antagonist, and LE300, a D\n                    <jats:sub>1<\/jats:sub>\n                    -like receptor antagonist. LE300 prevented the ability of FFB to increase gastrin protein expression in human G cells via the D\n                    <jats:sub>1<\/jats:sub>\n                    R, because the D\n                    <jats:sub>5<\/jats:sub>\n                    R, the other D\n                    <jats:sub>1<\/jats:sub>\n                    -like receptor, is not expressed in human G cells. Human G cells also express tyrosine hydroxylase and DOPA decarboxylase, enzymes needed to synthesize dopamine. G cells in the stomach may be the sodium sensor that stimulates gastrin secretion, which enables the kidney to eliminate acutely an oral sodium load. Dopamine, via the D\n                    <jats:sub>1<\/jats:sub>\n                    R, by interacting with PPAR-\u03b1, is involved in this process.\n                  <\/jats:p>","DOI":"10.1530\/jme-19-0053","type":"journal-article","created":{"date-parts":[[2019,12,3]],"date-time":"2019-12-03T11:43:49Z","timestamp":1575373429000},"page":"53-65","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":15,"title":["Stomach gastrin is regulated by sodium via PPAR-\u03b1 and dopamine D1 receptor"],"prefix":"10.1530","volume":"64","author":[{"given":"Peng","family":"Xu","sequence":"first","affiliation":[{"name":"1Department of Pathology, The University of Virginia, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John J","family":"Gildea","sequence":"additional","affiliation":[{"name":"1Department of Pathology, The University of Virginia, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chi","family":"Zhang","sequence":"additional","affiliation":[{"name":"1Department of Pathology, The University of Virginia, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prasad","family":"Konkalmatt","sequence":"additional","affiliation":[{"name":"2Division of Renal Diseases & Hypertension, Department of Medicine, The George Washington University, School of Medicine & Health Sciences, Washington, District of Columbia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Santiago","family":"Cuevas","sequence":"additional","affiliation":[{"name":"2Division of Renal Diseases & Hypertension, Department of Medicine, The George Washington University, School of Medicine & Health Sciences, Washington, District of Columbia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dora","family":"Bigler Wang","sequence":"additional","affiliation":[{"name":"1Department of Pathology, The University of Virginia, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanh T","family":"Tran","sequence":"additional","affiliation":[{"name":"1Department of Pathology, The University of Virginia, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pedro A","family":"Jose","sequence":"additional","affiliation":[{"name":"2Division of Renal Diseases & Hypertension, Department of Medicine, The George Washington University, School of Medicine & Health Sciences, Washington, District of Columbia, USA"},{"name":"3Department of Pharmacology and Physiology, The George Washington University, School of Medicine & Health Sciences, Washington, District of Columbia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robin A","family":"Felder","sequence":"additional","affiliation":[{"name":"1Department of Pathology, The University of Virginia, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Journal of Molecular Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/jme.bioscientifica.com\/view\/journals\/jme\/64\/2\/JME-19-0053.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/jme.bioscientifica.com\/downloadpdf\/journals\/jme\/64\/2\/JME-19-0053.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:53:43Z","timestamp":1784555623000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/jme\/article\/64\/2\/53-65\/14392"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2020,2]]},"references-count":0,"journal-issue":{"issue":"2"},"URL":"https:\/\/doi.org\/10.1530\/jme-19-0053","relation":{},"ISSN":["0952-5041","1479-6813"],"issn-type":[{"value":"0952-5041","type":"print"},{"value":"1479-6813","type":"electronic"}],"subject":[],"published":{"date-parts":[[2020,2]]}}}