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Oxidative stress in the etiology of age-associated decline in glucose metabolism

One of the most common pathologies in aging humans is the development of glucose metabolism dysfunction. The high incidence of metabolic dysfunction, in particular type 2 diabetes mellitus, is a significant health and economic burden on the aging population. However, the mechanisms that regulate thi...

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Detalles Bibliográficos
Autor principal: Salmon, Adam B
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922939/
https://www.ncbi.nlm.nih.gov/pubmed/24764512
http://dx.doi.org/10.1186/2046-2395-1-7
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author Salmon, Adam B
author_facet Salmon, Adam B
author_sort Salmon, Adam B
collection PubMed
description One of the most common pathologies in aging humans is the development of glucose metabolism dysfunction. The high incidence of metabolic dysfunction, in particular type 2 diabetes mellitus, is a significant health and economic burden on the aging population. However, the mechanisms that regulate this age-related physiological decline, and thus potential preventative treatments, remain elusive. Even after accounting for age-related changes in adiposity, lean mass, blood lipids, etc., aging is an independent factor for reduced glucose tolerance and increased insulin resistance. Oxidative stress has been shown to have significant detrimental impacts on the regulation of glucose homeostasis in vitro and in vivo. Furthermore, oxidative stress has been shown to be modulated by age and diet in several model systems. This review provides an overview of these data and addresses whether increases in oxidative stress with aging may be a primary determinant of age-related metabolic dysfunction.
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spelling pubmed-39229392014-02-14 Oxidative stress in the etiology of age-associated decline in glucose metabolism Salmon, Adam B Longev Healthspan Review One of the most common pathologies in aging humans is the development of glucose metabolism dysfunction. The high incidence of metabolic dysfunction, in particular type 2 diabetes mellitus, is a significant health and economic burden on the aging population. However, the mechanisms that regulate this age-related physiological decline, and thus potential preventative treatments, remain elusive. Even after accounting for age-related changes in adiposity, lean mass, blood lipids, etc., aging is an independent factor for reduced glucose tolerance and increased insulin resistance. Oxidative stress has been shown to have significant detrimental impacts on the regulation of glucose homeostasis in vitro and in vivo. Furthermore, oxidative stress has been shown to be modulated by age and diet in several model systems. This review provides an overview of these data and addresses whether increases in oxidative stress with aging may be a primary determinant of age-related metabolic dysfunction. BioMed Central 2012-11-01 /pmc/articles/PMC3922939/ /pubmed/24764512 http://dx.doi.org/10.1186/2046-2395-1-7 Text en Copyright © 2012 Salmon; 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
Salmon, Adam B
Oxidative stress in the etiology of age-associated decline in glucose metabolism
title Oxidative stress in the etiology of age-associated decline in glucose metabolism
title_full Oxidative stress in the etiology of age-associated decline in glucose metabolism
title_fullStr Oxidative stress in the etiology of age-associated decline in glucose metabolism
title_full_unstemmed Oxidative stress in the etiology of age-associated decline in glucose metabolism
title_short Oxidative stress in the etiology of age-associated decline in glucose metabolism
title_sort oxidative stress in the etiology of age-associated decline in glucose metabolism
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922939/
https://www.ncbi.nlm.nih.gov/pubmed/24764512
http://dx.doi.org/10.1186/2046-2395-1-7
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