| http://purl.uniprot.org/citations/9287040 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9287040 | http://www.w3.org/2000/01/rdf-schema#comment | "The selective impairment of glucose-induced insulin secretion in NIDDM can be attributed to defects in the glucose-signaling system. An alteration in the activity of phosphofructokinase (PFK), a key enzyme in the glycolytic pathway, may play a role in the abnormal glucose-induced insulin secretion. In this study, we evaluated insulin secretion in transgenic (Tg) mice overexpressing the liver-type subunit of phosphofructokinase (PFKL). Three independently derived Tg-PFKL lines showed random and postprandial hyperglycemia with diminished acute insulin response following intravenous glucose tolerance load. Isolated islets of Tg-PFKL mice exhibited a shift to the right of the glucose insulin dose curve. However, the maximal insulin secretory capacity, as well as the potentiation effect by arginine, were retained. PFK activity in Tg-PFKL islets was increased by 30-70%, because of the overexpression of PFKL. Conceivably, a selective overexpression of the PFKL isoform in Tg-PFKL mice altered the enzymatic properties of the tetrameric PFK and thereby affected glucose metabolism. A similar phenomenon was previously observed in transfected PC12-PFKL cells. The data show that overexpression of PFKL in transgenic mice was associated with diminished glucose-induced insulin response and suggest a mechanism to explain the role of beta-cell PFK activity in glucose-induced insulin secretion."xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.org/dc/terms/identifier | "doi:10.2337/diab.46.9.1414"xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/author | "Groner Y."xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/author | "Weiss Y."xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/author | "Knobler H."xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/author | "Peled M."xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/date | "1997"xsd:gYear |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/pages | "1414-1418"xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/title | "Impaired glucose-induced insulin response in transgenic mice overexpressing the L-phosphofructokinase gene."xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://purl.uniprot.org/core/volume | "46"xsd:string |
| http://purl.uniprot.org/citations/9287040 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/9287040 |
| http://purl.uniprot.org/citations/9287040 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/9287040 |
| http://purl.uniprot.org/uniprot/P12382#attribution-908A831E80699CDEAEC259A789C3799E | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/9287040 |
| http://purl.uniprot.org/uniprot/#_A0A1W2P7T1-mappedCitation-9287040 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9287040 |
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| http://purl.uniprot.org/uniprot/#_P12382-mappedCitation-9287040 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9287040 |
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| http://purl.uniprot.org/uniprot/A0A1W2P6Q4 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/9287040 |