http://purl.uniprot.org/citations/15677504 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/15677504 | http://www.w3.org/2000/01/rdf-schema#comment | "Carnitine palmitoyltransferase I, which is expressed in the pancreas as the liver isoform (LCPTI), catalyzes the rate-limiting step in the transport of fatty acids into the mitochondria for their oxidation. Malonyl-CoA derived from glucose metabolism regulates fatty acid oxidation by inhibiting LCPTI. To examine directly whether the availability of long-chain fatty acyl-CoA (LC-CoA) affects the regulation of insulin secretion in the beta-cell and whether malonyl-CoA may act as a metabolic coupling factor in the beta-cell, we infected INS(832/13) cells and rat islets with an adenovirus encoding a mutant form of LCPTI (Ad-LCPTI M593S) that is insensitive to malonyl-CoA. In Ad-LCPTI M593S-infected INS(832/13) cells, LCPTI activity increased sixfold. This was associated with enhanced fatty acid oxidation, at any glucose concentration, and a 60% suppression of glucose-stimulated insulin secretion (GSIS). In isolated rat islets in which LCPTI M593S was overexpressed, GSIS decreased 40%. The impairment of GSIS in Ad-LCPTI M593S-infected INS(832/13) cells was not recovered when cells were incubated with 0.25 mmol/l palmitate, indicating the deep metabolic influence of a nonregulated fatty acid oxidation system. At high glucose concentration, overexpression of a malonyl-CoA-insensitive form of LCPTI reduced partitioning of exogenous palmitate into lipid esterification products and decreased protein kinase C activation. Moreover, LCPTI M593S expression impaired K(ATP) channel-independent GSIS in INS(832/13) cells. The LCPTI M593S mutant caused more pronounced alterations in GSIS and lipid partitioning (fat oxidation, esterification, and the level of nonesterified palmitate) than LCPTI wt in INS(832/13) cells that were transduced with these constructs. The results provide direct support for the hypothesis that the malonyl-CoA/CPTI interaction is a component of a metabolic signaling network that controls insulin secretion."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.org/dc/terms/identifier | "doi:10.2337/diabetes.54.2.462"xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Hegardt F.G."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Asins G."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Serra D."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Sebastian D."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Herrero L."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Prentki M."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Maechler P."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/author | "Rubi B."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/pages | "462-471"xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/title | "Alteration of the malonyl-CoA/carnitine palmitoyltransferase I interaction in the beta-cell impairs glucose-induced insulin secretion."xsd:string |
http://purl.uniprot.org/citations/15677504 | http://purl.uniprot.org/core/volume | "54"xsd:string |
http://purl.uniprot.org/citations/15677504 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15677504 |
http://purl.uniprot.org/citations/15677504 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15677504 |
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http://purl.uniprot.org/uniprot/#_P97742-mappedCitation-15677504 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15677504 |
http://purl.uniprot.org/uniprot/#_Q7TQD5-mappedCitation-15677504 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15677504 |
http://purl.uniprot.org/uniprot/#_Q3UGT1-mappedCitation-15677504 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15677504 |
http://purl.uniprot.org/uniprot/P97742 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/15677504 |
http://purl.uniprot.org/uniprot/Q3UGT1 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/15677504 |
http://purl.uniprot.org/uniprot/Q7TQD5 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/15677504 |