Novel Pathway Reduces Diabetic Eye Disease in an Animal Model

Molecules known as Advanced Glycation End-Products (AGEs) are formed through sugar modifications given excess blood sugar levels in people with T1D. These products are known to be elevated in diabetes and can lead to inflammation. These AGEs have been implicated in the development of multiple T1D complications, including diabetic eye disease. This study shows that increased levels of the enzyme, glyoxalase can break down excess AGEs and reduce their accumulation in animal models. The reduced AGE levels help protect against diabetic eye disease in this animal model. This work supports the importance of AGEs in how complications develop in T1D, as well as suggests a way in which diabetic eye disease might be targeted with new therapies to prevent this complication.

Reference:

Berner AK, Brouwers O, Pringle R, Klaassen I, Colhoun L, McVicar C, Brockbank S, Curry JW, Miyata T, Brownlee M, Schlingemann RO, Schalkwijk C, Stitt AW. (2011). Protection against methylglyoxal-derived AGEs by regulation of glyoxalase 1 prevents retinal neuroglial and vasodegenerative pathology. Diabetologia. Dec 6. [Epub ahead of print]

Ramifications for Individuals with Type 1 Diabetes:

Targeting the enzyme glyoxalase may represent a viable way to reduce complications, including diabetic eye disease. There are currently no therapies available to directly augment glyoxalase activity. However, studying this pathway should reveal viable ways of targeting this system to protect against the complications of T1D.

JDRF Involvement:

JDRF supported this work via a grant to Dr. Alan Stitt.