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Postprandial hyperglycemia as an etiological factor in vascular failure

Postprandial hyperglycemia is characterized by hyperglycemic spikes that induce endothelial dysfunction, inflammatory reactions and oxidative stress, which may lead to progression of atherosclerosis and occurrence of cardiovascular events. Emerging data indicate that postprandial hyperglycemia or ev...

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Detalles Bibliográficos
Autores principales: Node, Koichi, Inoue, Teruo
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688503/
https://www.ncbi.nlm.nih.gov/pubmed/19402896
http://dx.doi.org/10.1186/1475-2840-8-23
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author Node, Koichi
Inoue, Teruo
author_facet Node, Koichi
Inoue, Teruo
author_sort Node, Koichi
collection PubMed
description Postprandial hyperglycemia is characterized by hyperglycemic spikes that induce endothelial dysfunction, inflammatory reactions and oxidative stress, which may lead to progression of atherosclerosis and occurrence of cardiovascular events. Emerging data indicate that postprandial hyperglycemia or even impaired glucose tolerance may predispose to progression of atherosclerosis and cardiovascular events. There is evidence that postprandial hyperglycemia, but not fasting hyperglycemia, independently predicts the occurrence of cardiovascular events. We proposed a concept of 'vascular failure' as a comprehensive syndrome of vascular dysfunction extending from risk factors to advanced atherosclerotic disease. Postprandial hyperglycemia is therefore one of the very important pathophysiological states contributing to vascular failure. Accordingly, controlling postprandial hyperglycemia should be the focus of future clinical investigation as a potential target for preventing vascular failure.
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spelling pubmed-26885032009-05-30 Postprandial hyperglycemia as an etiological factor in vascular failure Node, Koichi Inoue, Teruo Cardiovasc Diabetol Review Postprandial hyperglycemia is characterized by hyperglycemic spikes that induce endothelial dysfunction, inflammatory reactions and oxidative stress, which may lead to progression of atherosclerosis and occurrence of cardiovascular events. Emerging data indicate that postprandial hyperglycemia or even impaired glucose tolerance may predispose to progression of atherosclerosis and cardiovascular events. There is evidence that postprandial hyperglycemia, but not fasting hyperglycemia, independently predicts the occurrence of cardiovascular events. We proposed a concept of 'vascular failure' as a comprehensive syndrome of vascular dysfunction extending from risk factors to advanced atherosclerotic disease. Postprandial hyperglycemia is therefore one of the very important pathophysiological states contributing to vascular failure. Accordingly, controlling postprandial hyperglycemia should be the focus of future clinical investigation as a potential target for preventing vascular failure. BioMed Central 2009-04-29 /pmc/articles/PMC2688503/ /pubmed/19402896 http://dx.doi.org/10.1186/1475-2840-8-23 Text en Copyright © 2009 Node and Inoue; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Node, Koichi
Inoue, Teruo
Postprandial hyperglycemia as an etiological factor in vascular failure
title Postprandial hyperglycemia as an etiological factor in vascular failure
title_full Postprandial hyperglycemia as an etiological factor in vascular failure
title_fullStr Postprandial hyperglycemia as an etiological factor in vascular failure
title_full_unstemmed Postprandial hyperglycemia as an etiological factor in vascular failure
title_short Postprandial hyperglycemia as an etiological factor in vascular failure
title_sort postprandial hyperglycemia as an etiological factor in vascular failure
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688503/
https://www.ncbi.nlm.nih.gov/pubmed/19402896
http://dx.doi.org/10.1186/1475-2840-8-23
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