Diabetes mellitus (DM) is a group of metabolic diseases that presents as main characteristic the hyperglycemia that is generated by defects in insulin secretion. It is currently considered a worldwide epidemic, translating into major challenge for health systems worldwide. The increasing incidence of this disease is the result of an aging population, increasing urbanization, sedentary lifestyle, poor diet and obesity. This disease affects about 371 million people of 45-64 years around the world, just being in Brazil almost 13.4 million people. Among these patients about 30 to 60% presented some evidence tendinopathy. The constant hyperglycemia triggers increased chemical reactions that result in heightened production of Glycation End Products Advanced (Advanced Glycation End products - AGEs), derived from reactions between proteins and glucose or protein and fat. These may attach to the basement membrane extracellular matrix promoting a change in the formation of proteins such as collagen. The commitment tendon in patients with DM to date has been the subject of few studies and is extremely controversial in the literature. It is known that there are changes in the structure of the tendon and collagen synthesis derived from constant injury MD, leading to rupture of the tissue, but it is unknown to what extent these changes may reflect the biomechanics of tendon. Recently, was demonstrated that the increase of AGEs in the diabetic may interfere with tendon loss viscoelasticity, generating a sum of tissue damage. Although it was demonstrated that diabetic patients have an increased risk of foot ulcers due to increased glycation of collagen and consequent increase in tissue stiffness. On the other hand, we have demonstrated that diabetic rats ligaments have more fine fibers and that this fact could bring greater fragility of the tendon structure and consequently susceptibility to injury. Therefore, our proposal for this study will conduct a temporal analysis of fine fibers collagens (III and V) and evaluate its relationship with the formation of AGEs and the biomechanics of tendon in DM.
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