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Does Chronic Glycolysis Accelerate Aging? Could This Explain How Dietary Restriction Works?
Author(s) -
HIPKISS ALAN R.
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1354.051
Subject(s) - glycolysis , dihydroxyacetone , biochemistry , mitochondrion , glyceraldehyde 3 phosphate dehydrogenase , glyceraldehyde , methylglyoxal , chemistry , intracellular , dihydroxyacetone phosphate , reactive oxygen species , carnosine , senescence , microbiology and biotechnology , biology , metabolism , enzyme , dehydrogenase , glycerol
The mechanisms by which dietary restriction (DR) suppresses aging are not understood. Suppression of glycolysis by DR could contribute to controlling senescence. Many glycolytic intermediates can glycate proteins and other macromolecules. Methyglyoxal (MG), formed from dihydroxyacetone‐ and glyceraldehyde‐3‐phosphates, rapidly glycates proteins, damages mitochondria, and induces a prooxidant state to create a senescent‐like condition. Ad libitum ‐fed and DR animals differ in mitochondrial activity and glycolytic flux rates. Persistent glycolysis in the unrestricted condition would increase the intracellular load of glycating agents (e.g., MG) and increase ROS generation by inactive mitochondria. Occasional glycolysis during DR would decrease MG and reactive oxygen species (ROS) production and could be hormetic, inducing synthesis of glyoxalase‐1 and anti‐glycating agents (carnosine and polyamines).