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Publication

Glucose transporters in diabetic nephropathy.

Authors Brosius FC, Heilig CW Submitted By Frank Brosius on 2/23/2009 Status Published Journal Pediatric nephrology (Berlin, Germany) Year 2005 Date Published 4/1/2005 Volume : Pages 20(4) : 447 - 451 PubMed Reference 15717166 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 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
Name Institution Frank Brosius University of Arizona

Complications
All ComplicationsBioinformatics BoneCardiomyopathy CardiovascularGastro-Intestinal (GI) NephropathyNeuropathy & Neurocognition Pediatric Endocrinology Retinopathy UropathyWound Healing

Genes
Symbol Description Fn1 fibronectin 1 Jun Jun oncogene Prkca protein kinase C, alpha Slc1a3 solute carrier family 1, member 3 Slc2a1 solute carrier family 2 (facilitated glucose transporter), member 1