Glucose transporters in diabetic nephropathy
dc.contributor.author | Brosius, Frank C. | en_US |
dc.contributor.author | Heilig, Charles W. | en_US |
dc.date.accessioned | 2006-09-11T19:26:14Z | |
dc.date.available | 2006-09-11T19:26:14Z | |
dc.date.issued | 2005-04 | en_US |
dc.identifier.citation | Brosius, Frank C.; Heilig, Charles W.; (2005). "Glucose transporters in diabetic nephropathy." Pediatric Nephrology 20(4): 447-451. <http://hdl.handle.net/2027.42/47826> | en_US |
dc.identifier.issn | 0931-041X | en_US |
dc.identifier.issn | 1432-198X | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/47826 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15717166&dopt=citation | en_US |
dc.description.abstract | Changes in glucose transporter expression in glomerular cells occur early in diabetes. These changes, especially the GLUT1 increase in mesangial cells, appear to play a pathogenic role in the development of ECM expansion and perhaps other features of diabetic nephropathy. In addition, it appears that at least some diabetic patients may be predisposed to nephropathy because of polymorphisms in their GLUT1 genes. GLUT1 overexpression leads to increased glucose metabolic flux which in turn triggers the polyol pathway and activation of PKCα and Β1. Activation of these PKC isoforms can lead directly to AP-1 induced increases in fibronectin expression and ECM accumulation. Other, more novel effects of GLUT1 on cellular hypertrophy and injury could also promote changes of diabetic nephropathy. Strategies to prevent GLUT1 overexpression could ameliorate or prevent the progression of diabetic nephropathy. | en_US |
dc.format.extent | 166760 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Springer-Verlag; IPNA | en_US |
dc.subject.other | Mouse | en_US |
dc.subject.other | Type 1 Diabetes Mellitus | en_US |
dc.subject.other | Diabetic Nephropathy | en_US |
dc.subject.other | Podocyte | en_US |
dc.subject.other | Rat | en_US |
dc.subject.other | Reactive Oxygen Species | en_US |
dc.title | Glucose transporters in diabetic nephropathy | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbsecondlevel | Pediatrics | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Departments of Internal Medicine and Physiology, University of Michigan, 1150 W. Medical Center Dr., 1560 MSRB2, Ann Arbor, MI 48109-0676, USA | en_US |
dc.contributor.affiliationother | Departments of Medicine and Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 15717166 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/47826/1/467_2004_Article_1748.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/s00467-004-1748-x | en_US |
dc.identifier.source | Pediatric Nephrology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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