Cellular Glycation is a non-enzymatic chemical reaction where free reducing sugars, such as glucose, spontaneously bind to the amino groups of proteins, lipids, and nucleic acids within the cell. This detrimental process initiates a cascade that forms unstable Schiff bases and Amadori products, eventually leading to the formation of irreversible Advanced Glycation End products (AGEs). The accumulation of these products impairs cellular function and contributes significantly to the pathology of aging and metabolic diseases.
Origin
The term is derived from the biochemical process itself, specifically the Maillard reaction, which was first described in food chemistry but later recognized as a fundamental biological aging mechanism. In the context of endocrinology, the concept gained prominence with the understanding of hemoglobin A1c, a clinically measurable marker of long-term blood glucose control and protein glycation. This highlights the intimate link between glucose metabolism and tissue degradation.
Mechanism
The mechanism is initiated by hyperglycemia, which increases the availability of reactive sugar molecules to indiscriminately bind to cellular macromolecules. Once formed, AGEs disrupt protein structure and function, leading to cross-linking of structural proteins like collagen, resulting in tissue stiffness and loss of elasticity. Furthermore, AGEs bind to specific Receptors for AGEs (RAGE), triggering inflammatory and oxidative stress pathways that accelerate cellular senescence.
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