Aging and glycoxidant stress

Melpomeni Peppa; Jaime Uribarri; Helen Vlassara

doi:10.1007/bf03401503

Aging and glycoxidant stress

Melpomeni Peppa, Jaime Uribarri, Helen Vlassara

Research output: Contribution to journal › Review article › peer-review

73 Scopus citations

Abstract

Aging and related diseases are accompanied by increased Oxidative Stress (OS) and accumulation of Advanced Glycation End products (AGEs). One important component of AGEs accumulation with aging appears to be the sustained exposure to dietary AGE (dAGEs), which contributes to overloading of anti-AGE receptors and depletion of anti-oxidant reserves. In this review, we present experimental animal and human data which support this postulation. Lowering the content of AGEs in the normal diet significantly prevents AGEs accumulation and the increased OS caused by aging and also extends lifespan in mice. In humans, short-term trials indicate that a Low AGEs diet reduces oxidant burden and inflammatory markers. Long-term studies are in progress and will help establish definitive causality between age-related disease states and modern dietary practices in Western societies.

Original language	English
Pages (from-to)	123-132
Number of pages	10
Journal	Hormones
Volume	7
Issue number	2
DOIs	https://doi.org/10.1007/bf03401503
State	Published - 2008

Keywords

AGE receptors
AGEs
Advanced Glycation End products
Aging
Glycoxidant stress
Inflammation
Oxidative stress

Access to Document

10.1007/bf03401503

Cite this

@article{20af224e90be41efb96ee28d0a66f681,

title = "Aging and glycoxidant stress",

abstract = "Aging and related diseases are accompanied by increased Oxidative Stress (OS) and accumulation of Advanced Glycation End products (AGEs). One important component of AGEs accumulation with aging appears to be the sustained exposure to dietary AGE (dAGEs), which contributes to overloading of anti-AGE receptors and depletion of anti-oxidant reserves. In this review, we present experimental animal and human data which support this postulation. Lowering the content of AGEs in the normal diet significantly prevents AGEs accumulation and the increased OS caused by aging and also extends lifespan in mice. In humans, short-term trials indicate that a Low AGEs diet reduces oxidant burden and inflammatory markers. Long-term studies are in progress and will help establish definitive causality between age-related disease states and modern dietary practices in Western societies.",

keywords = "AGE receptors, AGEs, Advanced Glycation End products, Aging, Glycoxidant stress, Inflammation, Oxidative stress",

author = "Melpomeni Peppa and Jaime Uribarri and Helen Vlassara",

year = "2008",

doi = "10.1007/bf03401503",

language = "English",

volume = "7",

pages = "123--132",

journal = "Hormones",

issn = "1109-3099",

publisher = "Springer Verlag",

number = "2",

}

TY - JOUR

T1 - Aging and glycoxidant stress

AU - Peppa, Melpomeni

AU - Uribarri, Jaime

AU - Vlassara, Helen

PY - 2008

Y1 - 2008

N2 - Aging and related diseases are accompanied by increased Oxidative Stress (OS) and accumulation of Advanced Glycation End products (AGEs). One important component of AGEs accumulation with aging appears to be the sustained exposure to dietary AGE (dAGEs), which contributes to overloading of anti-AGE receptors and depletion of anti-oxidant reserves. In this review, we present experimental animal and human data which support this postulation. Lowering the content of AGEs in the normal diet significantly prevents AGEs accumulation and the increased OS caused by aging and also extends lifespan in mice. In humans, short-term trials indicate that a Low AGEs diet reduces oxidant burden and inflammatory markers. Long-term studies are in progress and will help establish definitive causality between age-related disease states and modern dietary practices in Western societies.

AB - Aging and related diseases are accompanied by increased Oxidative Stress (OS) and accumulation of Advanced Glycation End products (AGEs). One important component of AGEs accumulation with aging appears to be the sustained exposure to dietary AGE (dAGEs), which contributes to overloading of anti-AGE receptors and depletion of anti-oxidant reserves. In this review, we present experimental animal and human data which support this postulation. Lowering the content of AGEs in the normal diet significantly prevents AGEs accumulation and the increased OS caused by aging and also extends lifespan in mice. In humans, short-term trials indicate that a Low AGEs diet reduces oxidant burden and inflammatory markers. Long-term studies are in progress and will help establish definitive causality between age-related disease states and modern dietary practices in Western societies.

KW - AGE receptors

KW - AGEs

KW - Advanced Glycation End products

KW - Aging

KW - Glycoxidant stress

KW - Inflammation

KW - Oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=47949105383&partnerID=8YFLogxK

U2 - 10.1007/bf03401503

DO - 10.1007/bf03401503

M3 - Review article

C2 - 18477549

AN - SCOPUS:47949105383

SN - 1109-3099

VL - 7

SP - 123

EP - 132

JO - Hormones

JF - Hormones

IS - 2

ER -

Aging and glycoxidant stress

Abstract

Keywords

Access to Document

Fingerprint

Cite this