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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1996-2-14
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pubmed:abstractText |
The aim of the present investigation was to determine whether the subcellular distribution and insulin-stimulated translocation of the GLUT4 isoform of the glucose transporter are affected when GLUT4 is overexpressed in mouse skeletal muscle, and if the overexpression of GLUT4 alters maximal insulin-stimulated glucose transport and metabolism. Rates of glucose transport and metabolism were assessed by hind-limb perfusion in GLUT4 transgenic (TG) mice and non-transgenic (NTG) controls. Glucose-transport activity was determined under basal (no insulin), submaximal (0.2 m-unit/ml) and maximal (10 m-units/ml) insulin conditions using a perfusate containing 8 mM 3-O-methyl-D-glucose. Glucose metabolism was quantified by perfusing the hind limbs for 25 min with a perfusate containing 8 mM glucose and 10 m-units/ml insulin. Under basal conditions, there was no difference in muscle glucose transport between TG (1.10 +/- 0.10 mumol/h per g; mean +/- S.E.M.) and NTG (0.93 +/- 0.16 mumol/h per g) mice. However, TG mice displayed significantly greater glucose-transport activity during submaximal (4.42 +/- 0.49 compared with 2.69 +/- 0.33 mumol/h per g) and maximal (11.68 +/- 1.13 compared with 7.53 +/- 0.80 mumol/h per g) insulin stimulation. Nevertheless, overexpression of the GLUT4 protein did not alter maximal rates of glucose metabolism. Membrane purification revealed that, under basal conditions, plasma-membrane (approximately 12-fold) and intracellular-membrane (approximately 4-fold) GLUT4 protein concentrations were greater in TG than NTG mice. Submaximal insulin stimulation did not increase plasma-membrane GLUT4 protein concentration whereas maximal insulin stimulation increased this protein in both NTG (4.1-fold) and TG (2.6-fold) mice. These results suggest that the increase in insulin-stimulated glucose transport following overexpression of the GLUT4 protein is limited by factors other than the plasma-membrane GLUT4 protein concentration. Furthermore, GLUT4 overexpression is not coupled to glucose-metabolic capacity.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-1401086,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-1443111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-1445278,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-1556135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-1651337,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-1662910,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-1699426,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-2104834,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-2178971,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-2199436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-2205203,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-3510557,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-4348494,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-5135248,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-5413312,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-7407175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-7829503,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-7961994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-8048627,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-8135807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-8214051,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-8226728,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-8248251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-8460676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8546674-8486663
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0264-6021
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
313 ( Pt 1)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
133-40
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:8546674-Animals,
pubmed-meshheading:8546674-Biological Transport,
pubmed-meshheading:8546674-Cell Membrane,
pubmed-meshheading:8546674-Glucose,
pubmed-meshheading:8546674-Humans,
pubmed-meshheading:8546674-Insulin,
pubmed-meshheading:8546674-Intracellular Membranes,
pubmed-meshheading:8546674-Isomerism,
pubmed-meshheading:8546674-Membrane Proteins,
pubmed-meshheading:8546674-Mice,
pubmed-meshheading:8546674-Mice, Transgenic,
pubmed-meshheading:8546674-Monosaccharide Transport Proteins,
pubmed-meshheading:8546674-Muscle, Skeletal,
pubmed-meshheading:8546674-Stimulation, Chemical,
pubmed-meshheading:8546674-Subcellular Fractions
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pubmed:year |
1996
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pubmed:articleTitle |
Glucose transport and GLUT4 protein distribution in skeletal muscle of GLUT4 transgenic mice.
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pubmed:affiliation |
Experimental Diabetes, Metabolism, and Nutrition Section, DB/NIDDK National Institutes of Health, Bethesda, MD 20892-1420, USA.
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pubmed:publicationType |
Journal Article
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