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Article: Insulin signaling to the glomerular podocyte is critical for normal kidney function

TitleInsulin signaling to the glomerular podocyte is critical for normal kidney function
Authors
Issue Date2010
Citation
Cell Metabolism, 2010, v. 12 n. 4, p. 329-340 How to Cite?
AbstractDiabetic nephropathy (DN) is the leading cause of renal failure in the world. It is characterized by albuminuria and abnormal glomerular function and is considered a hyperglycemic "microvascular" complication of diabetes, implying a primary defect in the endothelium. However, we have previously shown that human podocytes have robust responses to insulin. To determine whether insulin signaling in podocytes affects glomerular function in vivo, we generated mice with specific deletion of the insulin receptor from their podocytes. These animals develop significant albuminuria together with histological features that recapitulate DN, but in a normoglycemic environment. Examination of "normal" insulin-responsive podocytes in vivo and in vitro demonstrates that insulin signals through the MAPK and PI3K pathways via the insulin receptor and directly remodels the actin cytoskeleton of this cell. Collectively, this work reveals the critical importance of podocyte insulin sensitivity for kidney function. © 2010 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/195490
ISSN
2015 Impact Factor: 17.303
2015 SCImago Journal Rankings: 11.842
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWelsh, GI-
dc.contributor.authorHale, LJ-
dc.contributor.authorEremina, V-
dc.contributor.authorJeansson, M-
dc.contributor.authorMaezawa, Y-
dc.contributor.authorLennon, R-
dc.contributor.authorPons, DA-
dc.contributor.authorOwen, RJ-
dc.contributor.authorSatchell, SC-
dc.contributor.authorMiles, MJ-
dc.contributor.authorCaunt, CJ-
dc.contributor.authorMcArdle, CA-
dc.contributor.authorPavenstädt, H-
dc.contributor.authorTavaré, JM-
dc.contributor.authorHerzenberg, AM-
dc.contributor.authorKahn, CR-
dc.contributor.authorMathieson, PW-
dc.contributor.authorQuaggin, SE-
dc.contributor.authorSaleem, MA-
dc.contributor.authorCoward, RJM-
dc.date.accessioned2014-02-28T06:12:14Z-
dc.date.available2014-02-28T06:12:14Z-
dc.date.issued2010-
dc.identifier.citationCell Metabolism, 2010, v. 12 n. 4, p. 329-340-
dc.identifier.issn1550-4131-
dc.identifier.urihttp://hdl.handle.net/10722/195490-
dc.description.abstractDiabetic nephropathy (DN) is the leading cause of renal failure in the world. It is characterized by albuminuria and abnormal glomerular function and is considered a hyperglycemic "microvascular" complication of diabetes, implying a primary defect in the endothelium. However, we have previously shown that human podocytes have robust responses to insulin. To determine whether insulin signaling in podocytes affects glomerular function in vivo, we generated mice with specific deletion of the insulin receptor from their podocytes. These animals develop significant albuminuria together with histological features that recapitulate DN, but in a normoglycemic environment. Examination of "normal" insulin-responsive podocytes in vivo and in vitro demonstrates that insulin signals through the MAPK and PI3K pathways via the insulin receptor and directly remodels the actin cytoskeleton of this cell. Collectively, this work reveals the critical importance of podocyte insulin sensitivity for kidney function. © 2010 Elsevier Inc.-
dc.languageeng-
dc.relation.ispartofCell Metabolism-
dc.titleInsulin signaling to the glomerular podocyte is critical for normal kidney function-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cmet.2010.08.015-
dc.identifier.pmid20889126-
dc.identifier.scopuseid_2-s2.0-77957657608-
dc.identifier.volume12-
dc.identifier.issue4-
dc.identifier.spage329-
dc.identifier.epage340-
dc.identifier.isiWOS:000282836800009-
dc.identifier.f10006364956-

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