Purchase this article with an account.
M. Saraswat, P. Y. Reddy, P. Suryanarayana, G. B. Reddy; Inhibition of Protein Glycation by Dietary Agents: Implications in the Prevention of Diabetic Ocular Complications. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2287.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Diabetes is now one of the most common non-communicable diseases globally. Without proper management diabetes can lead to various short-term and long-term complications including ocular complications such as cataract and retinopathy. Multiple biochemical pathways have been proposed to explain the pathogenesis of ocular complications of diabetes and increased formation of advanced glycation end-products (AGE) is predominant among them. Prevention of AGE formation and breaking of the existing AGE-crosslinks has been considered potential target for diabetic ocular complicatios. We have screened a large number of dietary sources for their potential to prevent AGE formation using in vitro protein glycation system.
In vitro protein glycation system was used to assess the antiglycating nature of the dietary agents using total lens soluble portion as model proteins and fructose as glycating agent. Antiglycating effect of dietary sources was assessed by measuring the AGE related fluorescence, protein carbonyl content and prevention of formation of high molecular weight aggregates. A total of 20 commonly consumed sources were studied and compared for their relative inhibitory effect in preventing AGE formation. The significance of in vitro antiglycating potential of most effective dietary sources was evaluated using streptozotocin (STZ)-induced diabetic cataract rat model.
A number of diet sources were found to be potent inhibitors of AGE based on various complimentary methods that assessed the antiglycating ability. Ginger was found to be one of the most effective antiglycating agents, which could bring down the AGE-related fluorescence (80%) and carbonyl content (70%) and also a significant reduction in the formation of AGE-mediated high molecular weight aggregates. Further, when fed to diabetic rats, ginger delayed the progression and maturation of diabetic cataract in a dose dependent manner (0.5-3% in the diet) when compared to non-treated diabetic rats.
These results underline the importance of dietary factors as AGE inhibitors, which may have implications in prevention or treatment of diabetic ocular problems.
This PDF is available to Subscribers Only