One of the consequences of high glucose level (hyperglycemia) is the accelerated formation of advanced glycation end products (AGEs). This results in abnormal build-up of those molecules. These products have a wide variety of effects on body enzymes, and proteins and cause a variety of serious pathologies and disease conditions. The potential importance of AGEs in relationship to diabetic complications is suggested by animal studies that demonstarted that AGE inhibitors decreased effects of diabetic microvascular disease in the eyes (retina), kidneys, and nerves. Briefly, the following are some of the major effects of AGEs:

1. AGES accumulate in diabetic neuropathy.
2. AGEs bind to a specific receptor (RAGE), which is located on cells of the immune system (macrophages and T cells), cells lining the blood vessels (endothelium), and vascular smooth muscle cells. The binding of AGE to the receptor, RAGE, results in damaging effects on those cells. The result is disease conditions known to be complications of diabetes (examples: atherosclerosis, end-stage renal disease and neuropathy). Antagonists of RAGE are being tested in diabetes in clinical trials.
3. In addition to receptor-mediated effects, AGEs can directly cross-link matrix proteins in between and outside the cells, decresing the elasticity of large blood vessels. That could be another mechanism to develop endothelial injury.
5. AGEs are found in increased amounts outside the cells of diabetic retinal vessels where they can cause damage (retinopathy)

A recent study on Japanese individuals has shown that a low carbohydrate diet (LCD) could reduce AGEs levels in otherwise healthy overweight and obese subjects. (Ref: http://www.ncbi.nlm.nih.gov/pubmed/19420913)