| pubmed-article:10205010 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C1383501 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0074554 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0085542 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0678226 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C1256369 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:10205010 | lifeskim:mentions | umls-concept:C0332206 | lld:lifeskim |
| pubmed-article:10205010 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:10205010 | pubmed:dateCreated | 1999-6-9 | lld:pubmed |
| pubmed-article:10205010 | pubmed:abstractText | 1. Hypercholesterolaemia often occurs in patients with type 2 diabetes, who therefore encounter administration of HMG-CoA reductase inhibitors. Alteration of pancreatic beta-cell function leading to an impaired insulin secretory response to glucose plays a crucial role in the pathogenesis of type 2 diabetes. Therefore, it is important to examine the effects of HMG-CoA reductase inhibitors on beta-cell function. 2. Cytosolic Ca2+ concentration ([Ca2+]i) plays a central role in the regulation of beta-cell function. The present study examined the effects of HMG-CoA reductase inhibitors on the glucose-induced [Ca2+]i signalling and insulin secretion in rat islet beta-cells. 3. Simvastatin, a lipophilic HMG-CoA reductase inhibitor, at 0.1-3 microg ml(-1) concentration-dependently inhibited the first phase increase and oscillation of [Ca2+]i induced by 8.3 mM glucose in single beta-cells. The less lipophilic inhibitor, simvastatin-acid, inhibited the first phase [Ca2+]i increase but was two orders of magnitude less potent. The hydrophilic inhibitor, pravastatin (100 microg ml(-1), was without effect on [Ca2+]i. 4. Simvastatin (0.3 microg ml(-1)), more potently than simvastatin-acid (30 microg ml(-1)), inhibited glucose-induced insulin secretion from islets, whereas pravastatin (100 microg ml(-1)) had no effect. 5. Whole-cell patch clamp recordings demonstrated a reversible inhibition of the beta-cell L-type Ca2+ channels by simvastatin, but not by pravastatin. Simvastatin also inhibited the [Ca2+]i increases by L-arginine and KCl, agents that act via opening of L-type Ca2+ channels. 6. In conclusion, lipophilic HMG-CoA reductase inhibitors can inhibit glucose-induced [Ca2+]i signalling and insulin secretion by blocking L-type Ca2+ channels in beta-cells, and their inhibitory potencies parallel their lipophilicities. Precaution should be paid to these findings when HMG-CoA reductase inhibitors are used clinically, particularly in patients with type 2 diabetes. | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10205010 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205010 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10205010 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:10205010 | pubmed:issn | 0007-1188 | lld:pubmed |
| pubmed-article:10205010 | pubmed:author | pubmed-author:ShiraishiTT | lld:pubmed |
| pubmed-article:10205010 | pubmed:author | pubmed-author:NakataMM | lld:pubmed |
| pubmed-article:10205010 | pubmed:author | pubmed-author:KakeiMM | lld:pubmed |
| pubmed-article:10205010 | pubmed:author | pubmed-author:YadaTT | lld:pubmed |
| pubmed-article:10205010 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10205010 | pubmed:volume | 126 | lld:pubmed |
| pubmed-article:10205010 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10205010 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10205010 | pubmed:pagination | 1205-13 | lld:pubmed |
| pubmed-article:10205010 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:meshHeading | pubmed-meshheading:10205010... | lld:pubmed |
| pubmed-article:10205010 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10205010 | pubmed:articleTitle | Inhibition by simvastatin, but not pravastatin, of glucose-induced cytosolic Ca2+ signalling and insulin secretion due to blockade of L-type Ca2+ channels in rat islet beta-cells. | lld:pubmed |
