Abstract
The net effect of euglycemic treatment is grossly overestimated in diabetes mellitus
and retinopathy, similar to what is observed in diabetic individuals, is found in
the absence of chronic hyperglycemia. Explanations of this clinical paradox include
the excess generation of reactive intermediates of metabolism. Excess formation or
impaired detoxification of reactive intermediates can also result in multiple posttranslational
modifications with a wide range of cellular dysfunctions. The multicellular neurovascular
unit represents the response element of the retina which is crucial for the development
of diabetic retinopathy. Current evidence suggests that increased reactive intermediates
in the retina induce (micro-)glial activation, neurodegeneration and vasoregression
similar to alterations found in the diabetic retina. Reactive metabolites can be lowered
by metabolic signal blockade, by an activation of detoxification pathways and by quenching.
The translation of these novel findings into treatment of patients with complications
is important to reduce individual suffering and financial burden for societies.
Quick Summary:Increased levels of reactive intermediates, independent of blood glucose
levels, are linked to damage of the neurovascular unit of the diabetic retina.
Key words
reactive metabolites - diabetic complications - diabetic retinopathy
