Glucose transporters in diabetic nephropathy

Frank C. Brosius, Charles W. Heilig

Research output: Contribution to journalReview articlepeer-review

51 Scopus citations

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 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.

Original languageEnglish (US)
Pages (from-to)447-451
Number of pages5
JournalPediatric Nephrology
Volume20
Issue number4
DOIs
StatePublished - Apr 2005
Externally publishedYes

Keywords

  • Diabetic nephropathy
  • Mouse
  • Podocyte
  • Rat
  • Reactive oxygen species
  • Type 1 diabetes mellitus

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Nephrology

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