Impaired glucose tolerance: Its relevance to early endothelial dysfunction


Konukoglu D. , DOĞAN E., Turhan M. S. , HATEMİ H.

HORMONE AND METABOLIC RESEARCH, vol.35, no.10, pp.607-610, 2003 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 35 Issue: 10
  • Publication Date: 2003
  • Doi Number: 10.1055/s-2003-43508
  • Title of Journal : HORMONE AND METABOLIC RESEARCH
  • Page Numbers: pp.607-610

Abstract

We studied the effects of acute glycemia on plasma nitric oxide (NO; nitrite plus nitrate) levels, Cu-Zn Superoxide dismutase (Cu-Zn SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels in age-matched female subjects before and tow hours after glucose loading. According to the results of glucose loading, subjects were divided in the three groups as normal (n = 13, NGT), impaired (n = 11, IGT) and diabetic glucose tolerance (n = 10, DGT). Plasma NO levels were significantly higher in subjects with DGT than in subjects with NGT (p < 0.001) and IGT (p < 0.05) at baseline. Two hours after glucose loading, plasma NO levels were significantly decreased in subjects with IGT and DGT (p < 0.001 and p < 0.001). Although plasma TBARS levels in subject with NGT did not change from the baseline levels after glucose loading, TBARS levels were significantly elevated in subjects with DGT and IGT (p < 0.001 and p < 0.001). Plasma Cu-Zn SOD activities were within a similar range in all subjects at baseline. Cu-Zn SOD activities were significantly increased in subjects with NGT, and were significantly decreased in subjects with IGT and DGT (p < 0.001 and p < 0.001) after glucose loading. There was a positive correlation between NO and glucose in subjects with NGT (r = 0.34, p < 0.01) and a negative correlation between NO and TBARS in IGT sum DGT during glucose tolerance (r= - 0.38, p < 0.01). We suggest that NO availability was decreased when the blood glucose levels were only moderately elevated above normal levels. This might be related with the enhanced oxidative stress.