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Incidence and prevalence of age-related type 2 diabetes mellitus and complications increasing markedly

(end-stage renal disease, loss of vision, myocardial infarction, stroke, peripheral vascular diseases and neuropathy) Diabetes mellitus affects not only the blood sugar levels, but also the lipid and protein metabolisms

Figure 55.1 Contribution of the aging process to the development of type 2 diabetes mellitus.

Incidence and prevalence of age-related type 2 diabetes mellitus and complications increasing markedly

(end-stage renal disease, loss of vision, myocardial infarction, stroke, peripheral vascular diseases and neuropathy) Diabetes mellitus affects not only the blood sugar levels, but also the lipid and protein metabolisms

Figure 55.1 Contribution of the aging process to the development of type 2 diabetes mellitus.

render proteins more susceptible to other attack such as oxidation. One of the best studied examples is LDL. OxLDL plays a pathogenic role in the development of atherosclerosis, by inducing an inflammatory process in the vessel wall.

Furthermore, the glycation can progress and lead to the formation of advanced age products (AGE) that can bind to their specific receptors (RAGE). RAGE are particularly present on endothelial cells, glomeruli, mesangial cells, and monocytes. This interaction leads to the activation of various signaling events intra-cellularly. The overall effect of AGE products is the production of pro-inflammatory signaling molecules such as TNF-a, IGF-I, and GM-CSF. They induce also the proliferation of the connective tissue including collagen type-IV, laminin, and proteoglycans. This production of connective tissue occurs mainly in the kidney glomeruli, in the retina, and in smooth muscle cells. The AGE products develop a chemotactic activity toward monocytes that will infiltrate various target tissues such as kidney, retina, and arterial wall. The AGE products were involved in the development of glomerulosclerosis, mesangial proliferation, monocyte infiltration, and thrombus formation. By these effects AGE products are recognized to be pro-inflammatory, adding their activities to those already well recognized in aging and type 2 diabetes.

One of the most important complications besides nephropathy is retinopathy. They share many common features. The diabetic retinopathy is characterized by the loss of pericytes and microaneurysm formation that contribute to the increased capillary permeability. These changes will progress following ischemia to proliferation of endothelial cells and capillaries hemorrhage. The absence of PDGF-B was incriminated to participate in pericyte death and endothelial proliferation. Moreover, some growth factors enriched intraocularly were also found to be contributing to the proliferating activity. IGF-I seems to play a major role in this context. The AGE-inhibitor aminoguanidine confirmed the role of AGEs specifically in the development of retinopathy.

The role of AGEs in diabetic complications was confirmed by the model of diabetic mice, in which the AGEs level was modulated either exogenously by the diet or endogenously by the administration of amino-guanidine. Furthermore, modulation of the AGE-R3 mediated processing and uptake of AGE in nonobese diabetic (NOD) mice confirmed the role of AGEs in the inflammatory process accompanying diabetes and its complications.

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