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J Diabetes Metab Disord ; 13(1): 9, 2014 Jan 07.
Artigo em Inglês | MEDLINE | ID: mdl-24398060

RESUMO

BACKGROUND: Hyperglycaemic load has been shown to cause endothelial dysfunction in patients diagnosed with diabetes mellitus or the pre-diabetic state of glucose intolerance. In the non-disease state such as in healthy subjects, the effect of glucose loading is still uncertain with conflicting results. The aim of this study was to test the hypothesis that an oral 75 g glucose load will not adversely attenuate the endothelial function of healthy participants, 2 hours postprandial. METHODS: This is a prospective single arm study evaluating the brachial artery flow-mediated vasodilation of 12 healthy participants before and after a 75 g glucose loading. Participants' age, body mass index, family history of diabetes, fasting blood glucose and 2 hour postprandial glucose levels were recorded. All data were analysed with SPSS 17.0 using Wilcoxon test. RESULTS: Primary analysis of the participants' brachial artery flow mediated vasodilation before and 2 hours after 75 g oral glucose loading did not show any statistically significant attenuation (p > 0.05) in brachial artery flow-mediated vasodilation, although a trend for reduction in endothelial relaxation was observed. Subgroup analysis of healthy participants with a positive family history of diabetes confirmed a statistically significant attenuation (p < 0.05) in brachial artery flow-mediated vasodilation after acute glucose loading even though the 2 hour postprandial blood glucose level, with a median value of 4.6 ± 2.2 mmol/L was within normal limits. This was not observed in the group without a positive family history of diabetes. CONCLUSION: Acute oral glucose loading significantly attenuates endothelial relaxation in healthy subjects with positive family history of diabetes but showed no effect in those without a positive family history of diabetes. The attenuation in endothelial relaxation was observed in the presence of normal glucose metabolism, suggesting a defect in endothelium relaxation even in the non-disease state in the group predisposed to diabetes.

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