4.1 Article

Acute hyperglycemia rapidly suppresses endothelium-dependent arterial dilation in first-degree relatives of type 2 diabetic patients

Journal

EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
Volume 116, Issue 2, Pages 112-117

Publisher

JOHANN AMBROSIUS BARTH VERLAG MEDIZINVERLAGE HEIDELBERG GMBH
DOI: 10.1055/s-2007-984478

Keywords

type 2 diabetes mellitus; first-degree relatives; endothelial dysfunction; acute hyperglycemia

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Objective: Previous studies showed that endothelium-dependent arterial dilation is impaired in first-degree relatives of type 2 diabetes in the fasting state. In the present study, we examined whether endothelial dysfunction occurs when acute hyperglycemia is induced by oral glucose loading in this cohort. Patients and Methods: This study included 32 normal glucose tolerant subjects. Of them, 17 with a family history (FH) of type 2 diabetic parents (FH+) and 15 with no first-degree relative with diabetes or coronary artery disease (FH-). The examination of vascular function was performed in fasting state and repeated 1 and 2 hours after a 75-g oral glucose loading by high resolution ultrasound. Results: Endothelium- dependent arterial dilation in FH+ group were significantly lower than those in FH- before and after oral glucose loading (5.12 +/- 0.61% vs 6.03 +/- 0.56%, fasting; 4.0 +/- 0.65% vs 5.70 +/- 0.42%, 1h; 4.43 +/- 0.61 % vs 5.82 +/- 0.67 % 2 h, p<0.05 each). In FH+ group, endothelium-dependent arterial dilation decreased significantly at 60min (4.0 0.65% vs 5.12 0.61%, p<0.01) and increased markedly from 60min at 120 min (4.43 +/- 0.61 % vs 4.0 +/- 0.65 %, p<0.05), which was still significantly lower than baseline (4.43 +/- 0.61% vs 5.12 +/- 0.61%, p<0.01). In FH- group, however, the arterial dilation did not differ significantly among the three time points (p > 0.05). In multiple regression analysis, endothelium-dependent arterial dilation was significantly correlated to FH+ (r = - 0.302, p<0.01). In addition, endothelium-dependent arterial dilation showed a correlation with plasma glucose (r= -0.460, p<0.01) and TBARS (r= -0.382, p<0.01) during OGTT in FH+ subjects. Conclusion: Significant endothelial dysfunction is present in the fasting state, hyperglycemia in response to oral glucose loading rapidly suppresses endothelium-dependent arterial dilation in FH+ subjects, probably through increased production of oxygen-derived free radicals.

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