Hypouricemia linked to an overproduction of nitric oxide is an early marker of oxidative stress in female subjects with type 1 diabetes

✍ Scribed by Dario Pitocco; Enrico Di Stasio; Federica Romitelli; Francesco Zaccardi; Barbara Tavazzi; Andrea Manto; Salvatore Caputo; Tittania Musella; Cecilia Zuppi; Stefano A. Santini; Giovanni Ghirlanda

• Publisher: John Wiley and Sons
• Year: 2008
• Tongue: English
• Weight: 118 KB
• Volume: 24
• Category: Article
• ISSN: 1520-7552
• DOI: 10.1002/dmrr.814

✦ Synopsis

Abstract

Objective

The aim of this study is to verify whether, early in the course of type 1 diabetes and assuming hyperglycemia as the only risk factor, women demonstrate a change in oxidative status due to an interaction between nitric oxide (NO) and uric acid production.

Methods

Thirty‐eight women with type 1 diabetes of less than 10 years' duration and with no diabetic complications were compared with 25 matched healthy female controls. Insulin, C‐peptide, NO, HbA~1c~ and oxidative stress metabolites were determined from venous blood samples taken from all patients after a 12 h overnight fast. Urine samples were used for urinary uric acid determination.

Results

Most oxidative stress metabolites were significantly increased (p < 0.0001), while plasmatic and urinary uric acid levels were significantly lower (p < 0.0001) in patients with type 1 diabetes compared with controls. Mean NO levels were inversely related to uricemia. Bivariate regression analysis showed a significant correlation between plasmatic uric acid and NO (p = 0.004), ascorbic acid (p = 0.042), triglycerides (p = 0.014) and HbA~1c~ (p < 0.0001). Linear multivariate regression analysis showed a significant relationship between HbA~1c~ and plasmatic uric acid (beta = − 0.465, p = 0.0004).

Conclusions

Oxidative stress is already present in the early stages of type 1 diabetes. We conclude that the initial increase in oxidative stress could be linked to a reduction in plasmatic levels of uric acid, which is probably directly caused by an overproduction of NO. Copyright © 2008 John Wiley & Sons, Ltd.