Glycated albumin promotes a generalized vasculopathy in the db/db mouse

Increased protein glycation has been mechanistically linked to accelerated vascular pathobiology in diabetes. Because glycated albumin induces biosynthetic abnormalities in cultured aortic endothelial cells that resemble those associated with macrovascular disease, we sought evidence that increased...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 1996-01, Vol.218 (1), p.72
Main Authors: Cohen, M P, Clements, R S, Cohen, J A, Shearman, C W
Format: Article
Language:English
Subjects:
Aging - physiology
Animals
Antibodies, Monoclonal - pharmacology
Biomarkers - blood
Blood Glucose - metabolism
Body Weight
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - physiopathology
Diabetic Angiopathies - physiopathology
Diabetic Angiopathies - prevention & control
Fibronectins - blood
Mice
Mice, Mutant Strains
Reference Values
Serum Albumin - immunology
Serum Albumin - toxicity
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Summary:Increased protein glycation has been mechanistically linked to accelerated vascular pathobiology in diabetes. Because glycated albumin induces biosynthetic abnormalities in cultured aortic endothelial cells that resemble those associated with macrovascular disease, we sought evidence that increased glycated albumin is operative in the genesis of diabetic vasculopathy in vivo. Plasma concentrations of fibronectin, a sensitive marker of endothelial cell damage, were increased two-fold in diabetic db/db mice compared with their nondiabetic db/m littermates. Treatment with monoclonal antibodies specifically reactive with albumin modified by Amadori glucose adducts normalized fibronectin in diabetic animals despite persistent hyperglycemia. These findings suggest that increased glycated albumin causally contributes to diabetic vasculopathy, and that blocking this influence ameliorates vascular damage.
ISSN:0006-291X
DOI:10.1006/bbrc.1996.0014