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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1992-8-24
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pubmed:abstractText |
Glucose-induced insulin secretion by beta cells of diabetic db/db mice was studied by a pancreas perfusion technique, and the levels of GLUT2 protein in pancreatic islets were assessed by immunofluorescence microscopy and protein blot analysis. Beta cells from diabetic mice had a high basal rate of insulin secretion; they did not respond to glucose stimulation but displayed a normal secretory response to arginine. At the same time, GLUT2 expression by db/db islets was lost whereas beta cells from nondiabetic db/+ mice expressed high levels of this transporter. GLUT2 levels in liver or kidney of diabetic mice were, however, mostly unaltered. Transplanting islets from db/db mice under the kidney capsule of db/+ mice restored normal GLUT2 levels. Conversely, transplantation of db/+ islets into db/db mice induced the disappearance of GLUT2 expression. When islets from db/+ mice were transplanted under the kidney capsule of streptozocin-diabetic mice, the immunodetection of GLUT2 also disappeared. We conclude that: (a) GLUT2 expression is decreased in glucose-unresponsive beta cells from db/db mice; (b) the decreased expression of GLUT2 is reversible; (c) the loss of GLUT2 expression is induced by the diabetic environment of db/db and streptozocin-induced diabetic mice. These observations together with previously published data suggest that a factor different from glucose or insulin regulates the beta cell expression of GLUT2.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-1701966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-1765007,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2006409,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2182619,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2190214,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2204056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2226113,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2237405,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2243134,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2260638,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2263645,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2312736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2407476,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2424696,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2602116,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-2665080,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-3048704,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-3540950,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-4373494,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-4374474,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-4552828,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-4693651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-5068062,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-5079926,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-6337325,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-6360782,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1634622-950363
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0021-9738
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
90
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
77-85
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
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pubmed:year |
1992
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pubmed:articleTitle |
The loss of GLUT2 expression by glucose-unresponsive beta cells of db/db mice is reversible and is induced by the diabetic environment.
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pubmed:affiliation |
Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142.
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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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