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Glucose transporters in diabetic nephropathy.
Brosius FC, Heilig CW
Frank Brosius on 2/23/2009
Pediatric nephrology (Berlin, Germany)
Volume : Pages
20(4) : 447 - 451
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 PKC alpha and B1. 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.
Investigators with authorship
University of Arizona
Neuropathy & Neurocognition
protein kinase C, alpha
solute carrier family 1, member 3
solute carrier family 2 (facilitated glucose transporter), member 1
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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