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
Frank BrosiusUniversity of Arizona


Fn1fibronectin 1
JunJun oncogene
Prkcaprotein kinase C, alpha
Slc1a3solute carrier family 1, member 3
Slc2a1solute carrier family 2 (facilitated glucose transporter), member 1