• Am. J. Med. · Apr 2015

    Reversal of hyperglycemia: effects on nitric oxide signaling.

    • Cher-Rin Chong, Saifei Liu, Giovanni Licari, Tamila Heresztyn, Yuliy Y Chirkov, Doan T Ngo, and John D Horowitz.
    • Cardiology and Clinical Pharmacology Department, Basil Hetzel Institute, the Queen Elizabeth Hospital, Woodville, South Australia, Australia; University of Adelaide, Adelaide, Australia.
    • Am. J. Med. 2015 Apr 1; 128 (4): 427430427-30.

    BackgroundHyperglycemia in patients with acute coronary syndromes is associated with poor outcomes, and its rapid correction with insulin infusion has been shown to restore platelet responsiveness to nitric oxide and to suppress superoxide (O2(-)) generation. Thioredoxin-interacting protein has emerged recently as a pivotal modulator of hyperglycemia-induced inflammation, O2(-) production, and impairment of nitric oxide signaling, but it is not known whether its expression in platelets can be downregulated rapidly.MethodsIn 12 hyperglycemic patients with acute coronary syndrome, we evaluated the putative role of thioredoxin-interacting protein suppression in the platelet nitric oxide response after reversal of hyperglycemia with insulin infusion.ResultsInsulin infusion for 13.0 ± 0.8 (standard error of the mean) hours decreased blood glucose level from 16.6 ± 1.6 mmol/L to 8.7 ± 1.4 mmol/L (P = .002). This induced (1) sensitization of antiaggregatory response to nitric oxide (from 6.5% ± 7.7% to 39.7% ± 7.0%, P < .0001); (2) improved endothelial progenitor cell function (from a median of 45 to 180 colony-forming units, P < .05); and (3) decreases of whole blood reactive oxygen species content (P < .05). However, there was no significant suppression of platelet thioredoxin-interacting protein expression (mean decrease, 59 arbitrary units; 95% confidence interval, -193 to +74).ConclusionsCorrection of hyperglycemia in patients with acute coronary syndrome rapidly reverses oxidative stress, restoring both platelet nitric oxide responsiveness and endothelial progenitor cell function, but this process is largely or entirely independent of thioredoxin-interacting protein.Copyright © 2015 Elsevier Inc. All rights reserved.

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