Glycation prevention
All diabetics know the meaning of HbA1c. It is glycated hemoglobin that provides information on three months average plasma glucose concentrations. The most recent studies prove, that anti-glycation is probably the most important effect of carnosine.
What is glycation?
Every second, a process called glycation (non-enzymatic glycosylation) takes place in the whole organism. This reaction can be described as the binding of a sugar (glucose or fructose) molecule to a protein or lipid molecule. Glycation changes the protein structure and thereby decreases the biological activity of this protein. Glycated proteins accumulated in the affected tissues are a reliable disease indicator. Many diseases linked to the age like vascular diseases, cataracts and some neurological diseases, are at least partly, glycation attributes. Carnosine as a glycation prevention substance, plays also an important role in the removal of glycated proteins. Carnosine binds with denatured molecules and allows the removal of glycated proteins from the cell.
Glycation, in biochemistry known as Maillard reaction, the formation of molecular compounds of glucose with vital biomolecules such as enzymes and other proteins, is another major cause of aging and possibly malignant tumors, including diabetes complications. Glucose is the “fuel” for glycation, the binding protein/glucose (including free radical formation) ends with the formation of advanced glycation endproducts (AGEs).
AGEs form cross-links, binding proteins together, reducing the flexibility and function of the tissues. The scientists claim that in fact no other molecule has such a toxic effect on proteins as AGEs. A huge amount of AGEs is produced in diabetes, considerably earlier than in healthy individuals. Glycation in diabetes is a process that completely disrupts normal organ functions, reducing their flexibility and role. Glycation was proved to be a diabetes-induced atherosclerosis factor. AGEs trigger a whole cascade of destructive processes when they bind to the cell structures. One of the consequences is that the formation of free radicals increased by 50 times. Diabetes produces accelerated aging, glycation and AGEs forming an attack on the lens, arteries, peripheral nerves and kidneys in particular. Preventing glycation moderates kidney damage and the following inflammatory and degenerative changes. Diabetic rats that have not been treated with glycation inhibitors have shown double AGEs caused damage of glomeruli compared to the control group treated with the inhibitors. Cataract - one of the diabetes complications - is also a consequence of the glycation. Glycation inhibitors, such as carnosine and calcium pyruvate, protect against this damage.
Supplementation of glycation inhibitors thus prevents many deviations that accompany the aging process. Because carnosine structurally involves glycation damaged sites, it must be sacrificed to spare the target. Carnosine also supports proteolytic (elimination of damaged, unuseful and often harmful proteins) pathways.
Carnosine with its anti-glycation effect can help with the prevention and treatment of diabetic complications like cataract, neuropathy, atherosclerosis and kidney failure.
