Key result
Acute hyperglycemia linked to ~30% lower endothelium-dependent arterial dilation in subjects with family history of T2D.
Why the study?
Endothelium-dependent arterial dilation is impaired in first-degree relatives of type 2 diabetes in the fasting state, but its response to acute hyperglycemia is unclear.
Does acute hyperglycemia induced by oral glucose loading suppress endothelium-dependent arterial dilation in first-degree relatives of type 2 diabetic patients?
Observational (n=32)
Does acute hyperglycemia induced by oral glucose loading suppress endothelium-dependent arterial dilation in first-degree relatives of type 2 diabetic patients?
Absolute Event Rate: 4% vs 5.7%
p-value: p=<0.05
Acute hyperglycemia rapidly suppresses endothelium-dependent arterial dilation in normal glucose tolerant subjects with a family history of type 2 diabetes, indicating early endothelial dysfunction.
Acute postprandial hyperglycemia may unmask endothelial dysfunction in first-degree T2D relatives; hypothesis-generating for vascular risk, prospective studies required.
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%, 1 h; 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 60 min (4.0+/-0.65% vs 5.12+/-0.61%, p<0.01) and increased markedly from 60 min 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.
No takes yet. Share an insight, caveat, or question.
Sun et al. (2008) conducted an observational in Normal glucose tolerance with family history of type 2 diabetes (n=32). Family history of type 2 diabetes (FH+) vs. No family history of diabetes or coronary artery disease (FH-) was evaluated on Endothelium-dependent arterial dilation at 1 hour post oral glucose loading (p=<0.05). Acute hyperglycemia induced by oral glucose loading rapidly suppressed endothelium-dependent arterial dilation in subjects with a family history of type 2 diabetes compared to controls (4.0% vs 5.70% at 1h, p<0.05).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: