Key result
Induced hyperglycemia links to rapid suppression of flow-mediated vasodilation in IGT and DM.
Why the study?
Chronic hyperglycemia causes endothelial dysfunction in diabetes, but many patients with type 2 diabetes or impaired glucose tolerance experience hyperglycemia only postprandially, prompting study into whether acute hyperglycemia induces endothelial dysfunction.
Population
58 subjects (17 with NGT, 24 with IGT, and 17 with type 2 DM)
Comparison
Oral glucose loading across NGT, IGT, and type 2 DM groups
Follow-up
2-h
Authors
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Physiological study reveals acute hyperglycemia rapidly impairs flow-mediated vasodilation in the brachial artery, indicating immediate vascular harm from elevated blood glucose.
Observational (n=58)
p-value: p=< 0.01
Kawano et al. (1999) conducted an observational in Type 2 diabetes mellitus and impaired glucose tolerance (n=58). Oral glucose loading vs. Fasting state was evaluated on Flow-mediated endothelium-dependent vasodilation (p=< 0.01). Hyperglycemia induced by oral glucose loading rapidly suppressed flow-mediated endothelium-dependent vasodilation, with significant decreases at 1 hour in IGT and DM groups (P<0.01 vs fasting).
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