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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0021641,
umls-concept:C0021670,
umls-concept:C0030685,
umls-concept:C0205251,
umls-concept:C0391871,
umls-concept:C0439849,
umls-concept:C0680255,
umls-concept:C1150444,
umls-concept:C1283071,
umls-concept:C1510827,
umls-concept:C1517499,
umls-concept:C1963578
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pubmed:issue |
15
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pubmed:dateCreated |
1994-5-19
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pubmed:abstractText |
The rat insulinoma cell line RIN 1046-38 loses glucose-stimulated insulin secretion as a function of time in culture. We found that the loss of glucose sensing in these cells was correlated with the loss of expression of GLUT-2 and glucokinase. Stable transfection of RIN cells with a plasmid containing the GLUT-2 cDNA conferred glucose-stimulated insulin release in intermediate but not high passage cells, with the near-maximal 3-fold increase occurring at 50 microM glucose. GLUT-2 expressing cells also exhibited a larger response to the combination of 5 mM glucose + 1 microM forskolin than untransfected cells (7.9 versus 1.6-2.7-fold, respectively). GLUT-2 expressing intermediate passage, but not high passage, RIN cells exhibited a 4-fold increase in glucokinase enzymatic activity relative to nonexpressing controls. Glucokinase activity was also increased by transfer of the GLUT-2 gene into intermediate passage RIN cells via recombinant adenovirus. Preincubation of GLUT-2 expressing intermediate passage RIN cells with 2-deoxyglucose to inhibit low Km hexokinases resulted in a glucose-stimulated insulin secretion response that was shifted toward the physiologic range. These studies indicate that GLUT-2 expression confers both a high and low affinity glucose-stimulated insulin secretion response to intermediate passage RIN cells.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3-O-Methylglucose,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Glucokinase,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 2,
http://linkedlifedata.com/resource/pubmed/chemical/Hexokinase,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Methylglucosides,
http://linkedlifedata.com/resource/pubmed/chemical/Monosaccharide Transport Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
269
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11523-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:8157682-3-O-Methylglucose,
pubmed-meshheading:8157682-Adenoviridae,
pubmed-meshheading:8157682-Animals,
pubmed-meshheading:8157682-Biological Transport,
pubmed-meshheading:8157682-Cell Line,
pubmed-meshheading:8157682-Forskolin,
pubmed-meshheading:8157682-Gene Expression,
pubmed-meshheading:8157682-Genetic Vectors,
pubmed-meshheading:8157682-Glucokinase,
pubmed-meshheading:8157682-Glucose,
pubmed-meshheading:8157682-Glucose Transporter Type 2,
pubmed-meshheading:8157682-Hexokinase,
pubmed-meshheading:8157682-Humans,
pubmed-meshheading:8157682-Insulin,
pubmed-meshheading:8157682-Insulinoma,
pubmed-meshheading:8157682-Kinetics,
pubmed-meshheading:8157682-Methylglucosides,
pubmed-meshheading:8157682-Monosaccharide Transport Proteins,
pubmed-meshheading:8157682-Pancreatic Neoplasms,
pubmed-meshheading:8157682-RNA, Messenger,
pubmed-meshheading:8157682-Rats,
pubmed-meshheading:8157682-Transfection,
pubmed-meshheading:8157682-Tumor Cells, Cultured
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pubmed:year |
1994
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pubmed:articleTitle |
GLUT-2 gene transfer into insulinoma cells confers both low and high affinity glucose-stimulated insulin release. Relationship to glucokinase activity.
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pubmed:affiliation |
Gifford Laboratories for Diabetes Research, University of Texas, Dallas 75235.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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