Effects of glucose tolerance on the changes provoked by glucose ingestion in microvascular function |
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Authors: | A Natali S Baldi F Vittone E Muscelli A Casolaro C Morgantini C Palombo E Ferrannini |
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Institution: | (1) Department of Internal Medicine, University of Pisa, Via Roma, 67, Pisa, 56100, Italy |
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Abstract: | Aims/hypothesis Hyperglycaemia and hyperinsulinaemia have opposite effects on endothelium-dependent vasodilatation in microcirculation, but
the net effect elicited by glucose ingestion and the separate influence of glucose tolerance are unknown.
Methods In participants with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) or diabetic glucose tolerance, multiple
plasma markers of both oxidative stress and endothelial activation, and forearm vascular responses (plethysmography) to intra-arterial
acetylcholine (ACh) and sodium nitroprusside (SNP) infusions were measured before and after glucose ingestion. In another
IGT group, we evaluated the time-course of the skin vascular responses (laser Doppler) to ACh and SNP (by iontophoresis) 1,
2 and 3 h into the OGTT; the plasma glucose profile was then reproduced by means of a variable intravenous glucose infusion
and the vascular measurements repeated.
Results Following oral glucose, plasma antioxidants were reduced by 5% to 10% (p < 0.01) in all patient groups. The response to acetylcholine was not affected by glucose ingestion in any group, while the
response to SNP was attenuated, particularly in the IGT group. The ACh:SNP ratio was slightly improved therefore in all groups,
even in diabetic participants, in whom it was impaired basally. A time-dependent improvement in ACh:SNP ratio was also observed
in skin microcirculation following oral glucose; this improvement was blunted when matched hyperglycaemia was coupled with
lower hyperinsulinaemia (intravenous glucose).
Conclusions/interpretation Regardless of glucose tolerance, oral glucose does not impair endothelium-dependent vasodilatation either in resistance arteries
or in the microcirculation, despite causing increased oxidative stress; the endogenous insulin response is probably responsible
for countering any inhibitory effect on vascular function. |
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Keywords: | Endothelium Glucose intolerance Hyperglycaemia Hyperinsulinaemia Microcirculation Nitric oxide Oxidative stress Resistance arteries Type 2 diabetes Vascular function |
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