U.S. Department of Energy

Pacific Northwest National Laboratory

Chelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications.

TitleChelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications.
Publication TypeJournal Article
Year of Publication2012
AuthorsNagai R, Murray DB, Metz TO, Baynes JW
JournalDiabetes
KeywordsAldehyde Reductase, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Animals, Antihypertensive Agents, Chelating Agents, Diabetes Complications, Glycosylation End Products, Advanced, Humans
Abstract

This article outlines evidence that advanced glycation end product (AGE) inhibitors and breakers act primarily as chelators, inhibiting metal-catalyzed oxidation reactions that catalyze AGE formation. We then present evidence that chelation is the most likely mechanism by which ACE inhibitors, angiotensin receptor blockers, and aldose reductase inhibitors inhibit AGE formation in diabetes. Finally, we note several recent studies demonstrating therapeutic benefits of chelators for diabetic cardiovascular and renal disease. We conclude that chronic, low-dose chelation therapy deserves serious consideration as a clinical tool for prevention and treatment of diabetes complications.

DOI10.2337/db11-1120
Alternate JournalDiabetes
PubMed ID22354928
PubMed Central IDPMC3282805
Grant ListDK071283 / DK / NIDDK NIH HHS / United States
DK19971 / DK / NIDDK NIH HHS / United States
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