pubmed-article:15220198 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15220198 | lifeskim:mentions | umls-concept:C0022131 | lld:lifeskim |
pubmed-article:15220198 | lifeskim:mentions | umls-concept:C2936399 | lld:lifeskim |
pubmed-article:15220198 | lifeskim:mentions | umls-concept:C0205419 | lld:lifeskim |
pubmed-article:15220198 | lifeskim:mentions | umls-concept:C2610946 | lld:lifeskim |
pubmed-article:15220198 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:15220198 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
pubmed-article:15220198 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
pubmed-article:15220198 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:15220198 | pubmed:dateCreated | 2004-6-28 | lld:pubmed |
pubmed-article:15220198 | pubmed:abstractText | Many metabolic factors affect the secretion of insulin from beta-cells and glucagon from alpha-cells of the islets of Langerhans to regulate blood glucose. Somatostatin from delta-cells, considered a local inhibitor of islet function, reduces insulin and glucagon secretion by activating somatostatin receptors in islet cells. Somatostatin secretion from delta-cells is increased by high glucose via glucose metabolism in a similar way to insulin secretion from beta-cells. However, it is unknown how low glucose triggers somatostatin secretion. Because L-glutamate is cosecreted with glucagon from alpha-cells under low-glucose conditions and acts as a primary intercellular messenger, we hypothesized that glutamate signaling triggers the secretion of somatostatin. In this study, we showed that delta-cells express GluR4c-flip, a newly identified splicing variant of GluR4, an (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type ionotropic glutamate receptor of rat. After treatment with L-glutamate, AMPA, or kainate, secretion of somatostatin from isolated islets was significantly stimulated under low-glucose conditions. The glutamate-dependent somatostatin secretion was Ca(2+) dependent and blocked by 6-cyano-7-nitroquinoxaline-2,3-dione. Somatostatin in turn inhibited the secretion of L-glutamate and glucagon from alpha-cells. These results indicate that L-glutamate triggers somatostatin secretion from delta-cells by way of the GluR4c-flip receptor under low-glucose conditions. The released somatostatin may complete the feedback inhibition of alpha-cells. Thus, alpha- and delta-cells may communicate with each other through L-glutamate and somatostatin signaling. | lld:pubmed |
pubmed-article:15220198 | pubmed:language | eng | lld:pubmed |
pubmed-article:15220198 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15220198 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:15220198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15220198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15220198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15220198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15220198 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15220198 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15220198 | pubmed:month | Jul | lld:pubmed |
pubmed-article:15220198 | pubmed:issn | 0012-1797 | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:KohDuk-SuDS | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:YamamotoAkits... | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:MoriyamaYoshi... | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:HayashiMitsuk... | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:UeharaShunsuk... | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:MuroyamaAkiko... | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:YatsushiroSho... | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:MorimotoRiyoR | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:MoritaMitsuhi... | lld:pubmed |
pubmed-article:15220198 | pubmed:author | pubmed-author:EchigoNorikoN | lld:pubmed |
pubmed-article:15220198 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15220198 | pubmed:volume | 53 | lld:pubmed |
pubmed-article:15220198 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15220198 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15220198 | pubmed:pagination | 1743-53 | lld:pubmed |
pubmed-article:15220198 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:15220198 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15220198 | pubmed:articleTitle | A novel variant of ionotropic glutamate receptor regulates somatostatin secretion from delta-cells of islets of Langerhans. | lld:pubmed |
pubmed-article:15220198 | pubmed:affiliation | Department of Biochemistry, Faculty of Pharmaceutical Sciences, Okayama University, Okayama 700-8530, Japan. moriyama@pheasant.pharm.okayama-u.ac.jp | lld:pubmed |
pubmed-article:15220198 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15220198 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:24797 | entrezgene:pubmed | pubmed-article:15220198 | lld:entrezgene |
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