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Mike Mitka

JAMA. 2005;293:148-149.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

An international team of researchers has resurrected a once-discarded theory to explain the mechanism underlying how chronic hyperglycemia in diabetes causes the microvascular complications that lead to diabetic retinopathy and other tissue problems. The findings, they say, may point to new avenues of research into novel therapies to treat such conditions.

Scientists from the United States and Denmark report that studies in laboratory rats bolster the idea that a primary cause of microvascular complications is chemically reactive, tissue-damaging free radicals and other chemical changes resulting from the increased transfer of electrons and protons from glucose to nicotinamide adenine dinucleotide (NAD) by a sequence of chemical reactions known as the sorbitol pathway (Diabetes. 2004;53:2931-2938).

Neovascularization of the disc is apparent in a patient with proliferative diabetic retinopathy. (Image from Gold DH, Lewis RA. Clinical Eye Atlas. Chicago, Ill: AMA Press; 2002.)

Joseph R. Williamson, MD, lead investigator . . . [Full Text of this Article]

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Reexamining the hyperglycemic pseudohypoxia hypothesis of diabetic oculopathy.
Diederen et al.
IOVS 2006;47:2726-2731.
ABSTRACT | FULL TEXT