New insights on non-enzymatic glycosylation may lead to therapeutic approaches for the prevention of diabetic complications.

It is generally accepted that chronic hyperglycaemia is responsible for most of the long-term complications of diabetes. Several studies suggest that accelerated non-enzymatic glycosylation may be the underlying mechanism by which hyperglycaemia causes complications. More recently, glucose auto-oxidation has been linked to non-enzymatic glycosylation, and glycosylated proteins have been shown to be a source of free radicals. These findings suggest the possibility that oxidative stress may be related to the development of diabetic complications. Anti-oxidants such as vitamins C and E have recently been demonstrated to reduce protein glycosylation both in vivo and in vitro. In addition they also act as scavengers of free radicals generated by non-enzymatic glycosylation of protein. These findings may lead to new therapeutic approaches for the prevention of complications by limiting the damage caused by non-enzymatic glycosylation and oxidant stress. Such therapies may also be useful in complementing existing treatment in those with the long-term complications of diabetes.