A review on prevention of glycation of proteins: Potential therapeutic substances to mitigate the severity of diabetes complications

Non-enzymatic reaction involving carbonyl of reducing sugars and amino groups in proteins produces advanced glycation end products (AGEs). AGE accumulation in vivo is a crucial factor in the progression of metabolic and pathophysiological mechanisms like obesity, diabetes, coronary artery disease, neurological disorders, and chronic renal failure. The body's own defense mechanism, synthetic inhibitors, and natural inhibitors can all help to prevent the glycation of proteins. Synthetic inhibitors have the potential to suppress the glycation of proteins through a variety of pathways. They could avoid Amadori product development by tampering with the addition of sugars to the proteins. Besides which, the free radical scavenging and blocking crosslink formation could be another mechanism behind their anti-glycation properties. In comparison with synthetic substances, naturally occurring plant products have been found to be comparatively non-toxic, cheap, and usable in an ingestible form. This review gives a brief introduction of the Maillard reaction; formation, characterization and pathology related to AGEs, potential therapeutic approaches against glycation, natural and synthetic inhibitors of glycation and their probable mechanism of action. The scientific community could get benefit from the combined knowledge about important molecules, which will further guide to the design and development of new pharmaceutical compounds.

Automated summary

Glycation of proteins plays a crucial role in the progression of various metabolic and pathophysiological mechanisms, and can be prevented through synthetic and natural inhibitors. Synthetic inhibitors can suppress protein glycation through multiple pathways, while naturally occurring plant products are non-toxic, cost-effective, and ingestible. This review provides an overview of the Maillard reaction, the formation and characterization of AGEs, potential therapeutic approaches against glycation, and the mechanisms of natural and synthetic inhibitors.