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Reversal of hyperglycemia: effects on nitric oxide signaling

Cher-Rin Chong1, Saifei Liu1, Giovanni Licari1

  • 1Cardiology and Clinical Pharmacology Department, Basil Hetzel Institute, the Queen Elizabeth Hospital, Woodville, South Australia, Australia; University of Adelaide, Adelaide, Australia.

The American Journal of Medicine
|December 3, 2014
PubMed
Abstract

Insights

Hyperglycemia correction in acute coronary syndrome rapidly improves nitric oxide response and endothelial function. However, this benefit is independent of changes in thioredoxin-interacting protein levels in platelets.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Biochemistry

Background:

  • Hyperglycemia in acute coronary syndromes (ACS) correlates with adverse outcomes.
  • Insulin infusion rapidly corrects hyperglycemia, improving platelet nitric oxide (NO) response and reducing superoxide generation.
  • Thioredoxin-interacting protein (TXNIP) is implicated in hyperglycemia-induced inflammation and oxidative stress, but its role in platelet function during ACS is unclear.

Purpose of the Study:

  • To investigate the role of thioredoxin-interacting protein (TXNIP) suppression in platelet nitric oxide (NO) response following hyperglycemia reversal in acute coronary syndrome (ACS) patients.
  • To assess the impact of insulin infusion on platelet TXNIP expression and NO signaling.

Main Methods:

  • Evaluated 12 hyperglycemic ACS patients receiving insulin infusion.
  • Measured changes in blood glucose, platelet nitric oxide responsiveness, endothelial progenitor cell function, and whole blood reactive oxygen species (ROS).
  • Assessed platelet thioredoxin-interacting protein (TXNIP) expression levels before and after insulin treatment.

Main Results:

  • Insulin infusion significantly decreased blood glucose levels (16.6 to 8.7 mmol/L).
  • Observed significant improvements in platelet nitric oxide (NO) response (6.5% to 39.7%) and endothelial progenitor cell function (45 to 180 CFU).
  • Reactive oxygen species (ROS) levels decreased, but platelet TXNIP expression showed no significant suppression.

Conclusions:

  • Rapid correction of hyperglycemia in ACS patients effectively reverses oxidative stress.
  • Restoration of platelet nitric oxide (NO) responsiveness and endothelial progenitor cell function occurs rapidly.
  • These beneficial effects are largely independent of changes in platelet thioredoxin-interacting protein (TXNIP) expression.
Keywords:
Acute coronary syndromeEndothelial progenitor cellHyperglycemiaNitric oxideOxidative stressThioredoxin-interacting protein

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