| pubmed-article:11988095 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11988095 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:11988095 | lifeskim:mentions | umls-concept:C0025519 | lld:lifeskim |
| pubmed-article:11988095 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:11988095 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:11988095 | lifeskim:mentions | umls-concept:C1413688 | lld:lifeskim |
| pubmed-article:11988095 | lifeskim:mentions | umls-concept:C1256369 | lld:lifeskim |
| pubmed-article:11988095 | pubmed:issue | Pt 1 | lld:pubmed |
| pubmed-article:11988095 | pubmed:dateCreated | 2002-5-3 | lld:pubmed |
| pubmed-article:11988095 | pubmed:abstractText | Lipid metabolism in the beta-cell is critical for the regulation of insulin secretion. Pancreatic beta-cells chronically exposed to fatty acids show higher carnitine palmitoyltransferase I (CPT I) protein levels, higher palmitate oxidation rates and an altered insulin response to glucose. We examined the effect of increasing CPT I levels on insulin secretion in cultured beta-cells. We prepared a recombinant adenovirus containing the cDNA for the rat liver isoform of CPT I. The overexpression of CPT I in INS1E cells caused a more than a 5-fold increase in the levels of CPT I protein (detected by Western blotting), a 6-fold increase in the CPT activity, and an increase in fatty acid oxidation at 2.5 mM glucose (1.7-fold) and 15 mM glucose (3.1-fold). Insulin secretion was stimulated in control cells by 15 mM glucose or 30 mM KCl. INS1E cells overexpressing CPT I showed lower insulin secretion on stimulation with 15 mM glucose (-40%; P<0.05). This decrease depended on CPT I activity, since the presence of etomoxir, a specific inhibitor of CPT I, in the preincubation medium normalized the CPT I activity, the fatty-acid oxidation rate and the insulin secretion in response to glucose. Exogenous palmitate (0.25 mM) rescued glucose-stimulated insulin secretion (GSIS) in CPT I-overexpressing cells, indicating that the mechanism of impaired GSIS was through the depletion of a critical lipid. Depolarizing the cells with KCl or intermediary glucose concentrations (7.5 mM) elicited similar insulin secretion in control cells and cells overexpressing CPT I. Glucose-induced ATP increase, glucose metabolism and the triacylglycerol content remained unchanged. These results provide further evidence that CPT I activity regulates insulin secretion in the beta-cell. They also indicate that up-regulation of CPT I contributes to the loss of response to high glucose in beta-cells exposed to fatty acids. | lld:pubmed |
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| pubmed-article:11988095 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11988095 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11988095 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11988095 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11988095 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11988095 | pubmed:month | May | lld:pubmed |
| pubmed-article:11988095 | pubmed:issn | 0264-6021 | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:WollheimClaes... | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:RubíBlancaB | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:HegardtFausto... | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:SerraDolorsD | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:AsinsGuillerm... | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:MaechlerPierr... | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:AntinozziPete... | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:IshiharaHisam... | lld:pubmed |
| pubmed-article:11988095 | pubmed:author | pubmed-author:HerreroLauraL | lld:pubmed |
| pubmed-article:11988095 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11988095 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11988095 | pubmed:volume | 364 | lld:pubmed |
| pubmed-article:11988095 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11988095 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11988095 | pubmed:pagination | 219-26 | lld:pubmed |
| pubmed-article:11988095 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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