advanced glycation end product 222 .pptx

AGEs

1. A dvanced G lycation E nd Products

2. Prolonged exposure to elevated glucose concentrations damages tissues by causing either to increased sorbitol pathway activity and glycosylation of proteins or cumulative irreversible formation of advanced glycosylation end products ( AGE ) on matrix proteins such as collagen and on nucleic acids and nucleoproteins.

3. Nonenzymatic glycation is a process by which glucose is chemically bound to amino groups of proteins but without the help of enzymes. During the process of glycation , early glycation products are formed first, which subsequently rearrange into final AGE structures through a series of very complex chemical reactions. Advanced Glycation End Products ( AGE)

4. BIOCHEMISTRY OF AGEs FORMATION AGEs can be formed exogenously and endogenously. EXOGENOUS SOURCES AGEs can be introduced into the body from the following sources; - Tobacco Smoke - Diet ENDOGENOUS SOURCES AGEs accumulate during the physiological aging process.

5. The body does have a defense against cross-linked proteins. The immune system has a receptor for AGEs. The macrophages engulf AGEs and Eventually the products are excreted in the urine AGE receptor

6. AGEs in diabetic vasculopathy and atherosclerosis LDL from the circulation binds to AGE-modified collagen of the blood vessel walls. (Vascular tissue AGE accumulation cause protein crosslinking & oxidative damage

7. AGEs and renal failure AGEs can induce an excess crosslinking of collagen molecules in the glomerular plasma membrane affecting the assembly and architecture of the glomerular basement membrane and mesangial matrix .

8. AGES and diabetic neuropathy and retinopathy In neuropathy Nonenzymatic glycation of axonal proteins causes alteration in structure and transport, leading to axonal atrophy and degeneration.. Axonal cytoskeletal proteins have essential roles in axonal structure and function. In retinopathy AGE-modified albumin co- localizes with the component of AGE receptors in the retinal vasculature