I

Amadori-type Advanced Glycosylation End Products (AGE)

Free Radicals

Specific Receptors (RAGE)

Figure 1 The production of AGEs. The interaction of AGEs with their specific receptors (RAGEs) generates free radicals.

cose is known to form glycosylation products with protein (Fig. 1). These Schiff bases rearrange and form more stable Amadori-type glycosylation end products (13). Some of these early glycosylation end products on collagen or proteins of the vessel wall undergo a complex series of chemical rearrangements to form irreversible advanced glycosylation end products (AGE). Receptors specific for AGEs (RAGE) have been identified on endothelial cells, monocytes, neurons, and smooth muscle cells (14-20). AGE-RAGE interaction induces free radicals (18).

The sorbitol pathway is another mechanism involved in glucotoxicity (21) (Fig. 2). Glucose is reduced to sorbitol by aldose reductase. Then sorbitol is oxidized by sorbitol dehydrogenase to fructose. The second reaction is coupled with the reduction of NAD+ to NADH (Fig. 1). The pathophysiological consequences are similar to changes during ischemia, and the increased NADH/NAD+ ratio has been termed pseudohypoxia (11). During hyperglycemia, the sorbitol pathway activity is increased. The increased ratio of NADH/

Aldosereductase

Sorbitoldehydrogenase

D-GIucose

Aldosereductase

Peripheral Neuropathy Natural Treatment Options

Peripheral Neuropathy Natural Treatment Options

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