Biogerontology

, Volume 5, Issue 6, pp 365–373

Glucose, glycation and aging

Review paper

DOI: 10.1007/s10522-004-3189-0

Cite this article as:
Suji, G. & Sivakami, S. Biogerontology (2004) 5: 365. doi:10.1007/s10522-004-3189-0

Abstract

Glycation, a deleterious form of post-translational modification of macromolecules has been linked to diseases such as diabetes, cataract, Alzheimer’s, dialysis related amyloidosis (DRA), atherosclerosis and Parkinson’s as well as physiological aging. This review attempts to summarize the data on glycation in relation to its chemistry, role in macromolecular damage and disease, dietary sources and its intervention. Macromolecular damage and biochemical changes that occur in aging and age-related disorders point to the process of glycation as the common event in all of them. This is supported by the fact that several age-related diseases show symptoms manifested by hyperglycemia. Free radical mediated oxidative stress is also known to arise from hyperglycemia. There is evidence to indicate that controlling hyperglycemia by antidiabetic biguanides prolongs life span in experimental animals. Caloric restriction, which appears to prolong life span by bringing about mild hypoglycemia and increased insulin sensitivity further strengthens the idea that glucose via glycation is the primary damaging molecule.

Keywords

AGEsagingcaloric restrictiondietglycationhyperglycemia

Abbreviations

AGEs

advanced glycation end products

CR

caloric restriction

CML

NÉ›-(carboxymethyl)lysine

HNE

4-hydroxy-2-nonenal

IRS

insulin receptor substrate

MRPs

maillard reaction products

MGO

methyl glyoxal

NEG

nonenzymatic glycation

RAGE

receptor for advanced glycation end products

ROS

reactive oxygen species

Copyright information

© Kluwer Academic Publishers 2004

Authors and Affiliations

  1. 1.Department of Life SciencesUniversity of MumbaiMumbaiIndia