Benfotiamine: a New Approach to Preventing Diabetic Retinopathy
March 3, 2003
Maintaining lower blood glucose levels is a critical and effective part of preventing diabetic retinopathy. Diabetes researchers would like to find ways to protect the retina even more. This study reveals a promising new possibility.
Diabetic retinopathy is a serious long-term complication of diabetes that can impair vision or even result in blindness. The condition develops when the retina of the eye is repeatedly exposed to high blood glucose levels (hyperglycemia). Research has shown that lower blood glucose levels can prevent or delay diabetic retinopathy. However, since even the best efforts may not prevent hyperglycemia completely, diabetes researchers are exploring ways to protect the retina when hyperglycemia occurs. A study published recently in the journal Nature Medicine was designed to find out whether a synthetic version of thiamine (vitamin B1) could prevent diabetic retinopathy despite high blood glucose levels.
The retina receives oxygen and other nutrients from the blood through a network of very small vessels. The inner lining of these vessels is composed of cells that can’t block the entry of glucose even when they have absorbed enough to meet their energy needs. When blood glucose levels are high, these cells continue to burn unneeded glucose, and waste products build up. The accumulation of waste sets off chemical reactions within the cells that damage, and eventually destroy, the retina’s blood vessels.
The first part of the study involved laboratory experiments to observe what happens when cells are exposed to excess glucose. The researchers focused on an enzyme called transketolase. Transketolase blocks the absorption of too much glucose into cells. Since transketolase requires thiamine to work, the researchers conducted tests to see whether extra thiamine could boost the effect of transketolase. It did, but with only minimal success. Next the team turned to a synthetic form of thiamine called benfotiamine, and repeated the experiments. This time transkeolase activity more than doubled, and prevented cell damage from exposure to high glucose levels.
These experiments suggested that benfotiamine might stop the process that leads to diabetic retinopathy. To find out, the researchers studied three groups of rats. Two of the groups included rats with diabetes and persistent hyperglycemia. Average weight and HbA1c levels were similar in both groups. The rats in only one of the two groups were fed benfotiamine. Treatment with benfotiamine did not affect weight or HbA1c levels. Both groups of rats with diabetes were compared to a group of rats without diabetes. All three groups were studied for 36 weeks.
At the end of the study, the research team examined all of the rats. The rats without diabetes had normal blood vessels in their retinas. The rats with diabetes that were not fed benfotiamine had severely damaged blood vessels that were clear evidence of diabetic retinopathy. The rats with diabetes that had received benfotiamine did not have retinopathy. In fact, their retinas appeared as healthy as those of the rats without diabetes.
The researchers conclude that benfotiamine prevented diabetic retinopathy in the experimental rats. These promising results cannot be applied to humans without additional research to determine effectiveness, safety and appropriate dosages. The authors recommend that such research begin promptly. Based on the findings of their study, the team is optimistic that prevention of diabetic retinopathy may become easier in the near future.
Hammes HP et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nature Medicine 2003; published online: 18 February 2003; doi:10.1038/nm834