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Regulation of glucose transporters in human peritoneal mesothelial cells

Michael Fischereder1, Bernd Schröppel, Patrick Wiese

  • 1Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany. michael.fischereder@klinik.uni-regensburg.de

Journal of Nephrology
|March 22, 2003
PubMed
Abstract

Insights

High glucose and cytokines increase glucose transporters (GLUTs) in mesothelial cells (MsC), potentially causing glucose toxicity during peritoneal dialysis. MsC cannot downregulate GLUTs, leading to higher intracellular glucose levels.

Area of Science:

  • Cell Biology
  • Nephrology
  • Biochemistry

Background:

  • Peritoneal fibrosis and mesothelial cell (MsC) injury in continuous ambulatory peritoneal dialysis (CAPD) are linked to infections and dialysate bioincompatibility, including high glucose.
  • Investigating the role of facilitative glucose transporters (GLUTs) in MsC is crucial for understanding glucose toxicity.

Purpose of the Study:

  • To examine the expression of GLUTs in MsC under conditions mimicking CAPD.
  • To determine if high glucose concentrations in dialysate affect glucose uptake and transporter expression in MsC.

Main Methods:

  • MsC were incubated with high glucose (60 mM), glucose/mannitol mixtures, PD effluent, or cytokine mix.
  • GLUT1, GLUT3, and SGLT expression was analyzed using RNase protection assay.
  • 14C-fluoro-deoxy-glucose uptake and kinetic studies (Vmax, Km) were performed to measure glucose transport.

Main Results:

  • High glucose significantly increased GLUT1 (1.4-fold) and GLUT3 (1.7-fold) mRNA expression in MsC.
  • Cytokine mix also stimulated GLUT1 (3-fold) and GLUT3 (1.7-fold) expression.
  • Increased glucose uptake was observed in 30 mM and 60 mM glucose, with a Km of approximately 3.7 mM.

Conclusions:

  • High ambient glucose concentrations and cytokines induce GLUT mRNA expression and glucose uptake in MsC.
  • MsC exhibit an inability to downregulate GLUTs, unlike other cells, potentially leading to increased intracellular glucose.
  • Elevated intracellular glucose during CAPD may contribute to MsC dysfunction and glucose toxicity.

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