Abstract

IN this seminar we review recent studies suggesting that the central pathologic features of diabetic complications are caused by the hyperglycemia-accelerated formation of nonenzymatic advanced glycosylation end products in tissue. We will emphasize new research findings with important clinical implications, since older information is available in previously published reviews.1 , 2 Other biochemical mechanisms by which hyperglycemia may contribute to the development of diabetic complications are not discussed here, since they are comprehensively reviewed elsewhere.3 4 5 6 7 8 Differences between Early and Advanced Glycosylation ProductsThe central pathophysiologic features of diabetic vascular complications are an abnormal leakage of proteins from the circulation and a progressive . . .

Keywords

MedicineGlycosylationAdvanced glycation end-productDiabetes mellitusPathophysiologyIntensive care medicineGlycationBioinformaticsPathologyEndocrinologyBiochemistryBiology

MeSH Terms

AnimalsDiabetes ComplicationsDiabetes MellitusGlycosylationHumans

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Publication Info

Year
1988
Type
review
Volume
318
Issue
20
Pages
1315-1321
Citations
2518
Access
Closed

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2518
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36
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1759
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Cite This

Jeffrey S. Flier, Lisa H. Underhill, Michael Brownlee et al. (1988). Advanced Glycosylation End Products in Tissue and the Biochemical Basis of Diabetic Complications. New England Journal of Medicine , 318 (20) , 1315-1321. https://doi.org/10.1056/nejm198805193182007

Identifiers

DOI
10.1056/nejm198805193182007
PMID
3283558

Data Quality

Data completeness: 81%