ABSTRACT It is suggested that excessive glycolysis within erythrocytes can promote the accumulation of methylglyoxal (MG) precursor dihydroxyacetone phosphate resulting from excessive catalytic activity of triosephosphate isomerase (TPI) which causes deamidation of TPI asparagine residues and eventual decline in catalytic activity. Consequently under conditions of excessive and continuous carbohydrate intake, and consequent high red cell glycolysis, it is suggested that the highly glycolytic erythrocytes could be a metabolic “Achilles’ heel,” not only accumulating MG but also delivering MG throughout the body.
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