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http://purl.uniprot.org/citations/27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27423314http://www.w3.org/2000/01/rdf-schema#comment"Mosapride, a gastrointestinal prokinetic drug, is an agonist of 5-hydroxytryptamine (5-HT) receptor 4 that also reduces blood glucose. Whether 5-HT4 receptor is distributed in pancreatic islets and whether mosapride can directly stimulate insulin secretion is unclear. In the present study, the protein expression and cellular location of 5-HT4 receptor in pancreas was detected through western blotting and immunofluorescence. The acute effects of 5-HT4 receptor agonists, mosapride and prucalopride, on insulin secretion were investigated in vivo and in vitro in normal and alloxan-induced diabetes rats. The results indicated that 5-HT4 receptor immunoreactivity was co-existed in the islets insulin-immunoreactive cells of rat, mouse, pig and human. However the immunoreactive cells of insulin and 5-HT4 receptor and the protein expression of 5-HT4 receptor were significantly decreased in the pancreas of alloxan-induced diabetes rats. In normal rats, mosapride and prucalopride decreased blood glucose and increased insulin secretion during glucose tolerance test, in association with an increase in glucose-stimulated insulin secretion, which was abolished by the 5-HT4 receptor antagonist GR113808. In diabetes rats, mosapride and prucalopride failed to improve blood glucose and insulin levels in the group of 180mg/kg alloxan, but increased glucose-stimulated insulin secretion in the group of 120mg/kg alloxan in vitro. We conclude that 5-HT4 receptor is distributed in the islet β cell. Activation of 5-HT4 receptor is able to stimulate insulin secretion directly, thereby reduce blood glucose. The study provides important experimental evidences for the 5-HT4 receptor regulating insulin secretion and acting as a potential drug target in diabetes treatment."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.org/dc/terms/identifier"doi:10.1016/j.ejphar.2016.07.024"xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Chen H."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Hong F."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Zheng L.F."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Zhu J.X."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/author"Yao Y.S."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/name"Eur J Pharmacol"xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/pages"354-361"xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/title"Activation of islet 5-HT4 receptor regulates glycemic control through promoting insulin secretion."xsd:string
http://purl.uniprot.org/citations/27423314http://purl.uniprot.org/core/volume"789"xsd:string
http://purl.uniprot.org/citations/27423314http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27423314
http://purl.uniprot.org/citations/27423314http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27423314
http://purl.uniprot.org/uniprot/#_A0A9K3Y826-mappedCitation-27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27423314
http://purl.uniprot.org/uniprot/#_A0A494BA82-mappedCitation-27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27423314
http://purl.uniprot.org/uniprot/#_C4WYH1-mappedCitation-27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27423314
http://purl.uniprot.org/uniprot/#_C4WYH2-mappedCitation-27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27423314
http://purl.uniprot.org/uniprot/#_C4WYH3-mappedCitation-27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27423314
http://purl.uniprot.org/uniprot/#_A6IXJ7-mappedCitation-27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27423314
http://purl.uniprot.org/uniprot/#_A6IXJ8-mappedCitation-27423314http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27423314