File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The human glomerular podocyte is a novel target for insulin action

TitleThe human glomerular podocyte is a novel target for insulin action
Authors
Issue Date2005
Citation
Diabetes, 2005, v. 54 n. 11, p. 3095-3102 How to Cite?
AbstractMicroalbuminuria is significant both as the earliest stage of diabetic nephropathy and as an independent cardiovascular risk factor in nondiabetic subjects, in whom it is associated with insulin resistance. The link between disorders of cellular insulin metabolism and albuminuria has been elusive. Here, we report using novel conditionally immortalized human podocytes in vitro and human glomeruli ex vivo that the podocyte, the principal cell responsible for prevention of urinary protein loss, is insulin responsive and able to approximately double its glucose uptake within 15 min of insulin stimulation. Conditionally immortalized human glomerular endothelial cells do not respond to insulin, suggesting that insulin has a specific effect on the podocyte in the glomerular filtration barrier. The insulin response of the podocyte occurs via the facilitative glucose transporters GLUT1 and GLUT4, and this process is dependent on the filamentous actin cytoskeleton. Insulin responsiveness in this key structural component of the glomerular filtration barrier may have central relevance for understanding of diabetic nephropathy and for the association of albuminuria with states of insulin resistance. © 2005 by the American Diabetes Association.
Persistent Identifierhttp://hdl.handle.net/10722/195433
ISSN
2015 Impact Factor: 8.784
2015 SCImago Journal Rankings: 5.185
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCoward, RJM-
dc.contributor.authorWelsh, GI-
dc.contributor.authorYang, J-
dc.contributor.authorTasman, C-
dc.contributor.authorLennon, R-
dc.contributor.authorKoziell, A-
dc.contributor.authorSatchell, S-
dc.contributor.authorHolman, GD-
dc.contributor.authorKerjaschki, D-
dc.contributor.authorTavaré, JM-
dc.contributor.authorMathieson, PW-
dc.contributor.authorSaleem, MA-
dc.date.accessioned2014-02-28T06:12:08Z-
dc.date.available2014-02-28T06:12:08Z-
dc.date.issued2005-
dc.identifier.citationDiabetes, 2005, v. 54 n. 11, p. 3095-3102-
dc.identifier.issn0012-1797-
dc.identifier.urihttp://hdl.handle.net/10722/195433-
dc.description.abstractMicroalbuminuria is significant both as the earliest stage of diabetic nephropathy and as an independent cardiovascular risk factor in nondiabetic subjects, in whom it is associated with insulin resistance. The link between disorders of cellular insulin metabolism and albuminuria has been elusive. Here, we report using novel conditionally immortalized human podocytes in vitro and human glomeruli ex vivo that the podocyte, the principal cell responsible for prevention of urinary protein loss, is insulin responsive and able to approximately double its glucose uptake within 15 min of insulin stimulation. Conditionally immortalized human glomerular endothelial cells do not respond to insulin, suggesting that insulin has a specific effect on the podocyte in the glomerular filtration barrier. The insulin response of the podocyte occurs via the facilitative glucose transporters GLUT1 and GLUT4, and this process is dependent on the filamentous actin cytoskeleton. Insulin responsiveness in this key structural component of the glomerular filtration barrier may have central relevance for understanding of diabetic nephropathy and for the association of albuminuria with states of insulin resistance. © 2005 by the American Diabetes Association.-
dc.languageeng-
dc.relation.ispartofDiabetes-
dc.titleThe human glomerular podocyte is a novel target for insulin action-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.2337/diabetes.54.11.3095-
dc.identifier.pmid16249431-
dc.identifier.scopuseid_2-s2.0-32244446658-
dc.identifier.volume54-
dc.identifier.issue11-
dc.identifier.spage3095-
dc.identifier.epage3102-
dc.identifier.isiWOS:000233023100005-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats