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Mechanisms underlying endothelial dysfunction in diabetes mellitus.

U Hink1, H Li, H Mollnau

  • 1Universitätskrankenhaus Eppendorf, Germany.

Circulation Research
|February 7, 2001
PubMed
Summary

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High glucose activates protein kinase C (PKC) and nitric oxide synthase (NOS III) in diabetes, increasing superoxide. PKC inhibitors restored nitric oxide bioavailability and endothelial function in diabetic rats.

Area of Science:

  • Vascular biology
  • Endocrinology
  • Biochemistry

Background:

  • High glucose in diabetes activates protein kinase C (PKC) and nitric oxide synthase (NOS III), increasing superoxide production.
  • Mechanisms underlying these changes in endothelial cells remain unclear.

Purpose of the Study:

  • To investigate the in vivo mechanisms of endothelial dysfunction in diabetes.
  • To explore the role of protein kinase C (PKC) in mediating diabetes-induced vascular changes.

Main Methods:

  • Diabetes was induced in rats using streptozotocin.
  • Vascular superoxide production, nitric oxide bioavailability, and NOS III gene expression were assessed.
  • Inhibition of PKC and NOS was performed in vitro and in vivo.

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Main Results:

  • Diabetic rats showed endothelial dysfunction and increased vascular superoxide production.
  • Despite increased NOS III expression, nitric oxide bioavailability was reduced.
  • PKC inhibition reduced vascular superoxide in diabetic vessels and normalized NOS III gene expression and superoxide production in vivo, restoring endothelial function.

Conclusions:

  • Protein kinase C (PKC) plays a critical role in mediating diabetes-induced vascular complications.
  • PKC inhibitors show therapeutic potential for preventing or treating vascular complications in diabetes mellitus.